Ill]W11Ifllflflrfllflufllflfllfll”MW THEs-v LIBRAR Y Michigan State Universe » v This is to certify that the thesis entitled PARTITIONING OF COLLATERAL RESISTANCE IN EXCISED DOG LUNGS presented by Masaudsherif Rahouma Mukhtar has been accepted towards fulfillment of the requirements for M- 2:. degree in My Major professor Date 6/28/79 0-7639 OVERDUE FINES ARE 25¢ PER DAY PER ITEM Return to book drop to remove this checkout from your record. PARTITIONING 0F COLLATERAL RESISTANCE IN EXCISED DOG LUNGS By Masaudsherif Rahouma Mukhtar A THESIS Submitted to Michigan State University in partial fulfillment of the requirements for the degree of MASTER OF SCIENCE Department of Physiology 1979 ABSTRACT PARTITIONING OF COLLATERAL RESISTANCE IN EXCISED DOG LUNGS By Masaudsherif Rahouma Mukhtar A double Lumen catheter was advanced through the main bronchus so that an airway was obstructed and a sublobar segment was isolated. Collateral flow entered through the outer Lumen while the inner Lumen used was to measure pressure at the site of obstruction. Resistance (Rcoll) to collateral flow (Vcoll) was given by the formula Two additional catheters were inserted through the pleural surface in order to measure pressure in the isolated segment and extrasegmently so that resistance could be partitioned. Catheters were also inserted at different places in the obstructed segment to partition resistance between multiple sites in the segment. Pressure volume (P-V) curves were obtained so that Rcoll could be evaluated as the percentage of total lobe capacity (TLC). Collateral resistance was partitioned at lobar inflating pressure Masaudsherif Rahouma Mukhtar (PL) = 2.5, 5, 10, TE, 20 and 25 cm H20 during both inflation and deflation. Collateral resistance increases as PL decreases and segmental airway resistance accounts for approximately 30% of the total collateral resistance. Inflation Rcoll was higher than deflation Rcoll when resistance was expressed as a function of PL, however it was less than deflation Rcoll below 75% TLC when resist- ance was expressed as a function of percentage TLC. The behavior of the Rcoll suggests peripheral pathways as the site of resist- ance measurements. The segment airway component was dependent on the position of the parenchymal catheter. ACKNOWLEDGMENTS I greatly appreciate the guidance and help of my academic advisor, professor N. E. Robinson throughout my master's program. For their time and effort in serving on my committee and for critically reading this manuscript, no less appreciation goes to professor J. Hoffert and professor L. E. Wolternik. Last but not least, I express my thanks to Ms. Roberta Milar for her cheerful support and faithful technical assistance. ii TABLE OF CONTENTS ACKNOWLEDGMENTS . LIST OF TABLES LIST OF FIGURES . Chapter I. II. III. INTRODUCTION AND LITERATURE REVIEW Historical Development . . Possible Pathways for Collateral Ventilation . Factors Affecting Collateral Ventilation Techniques Used to Study Collateral Ventilation : Partitioning of Pulmonary Resistance MATERIALS AND METHODS Surgical Preparation . . . Isolation of a Segment of Lobe . . Partitioning of Collateral Resistance Lobar Pressure Volume Curves Measurement of Minimal Volume . Measurement of Segmental Volume Measure of Pressure at Multiple Sites in the Segment RESULTS Effect of Inflation Pressure (PL) and Volume History on Lobe Collateral Resistance . . Collateral Resistance as a Function of TLC Measurement of Pressure at Different Sites in the Segment Lobar Volume iii Page ii iv 36 38 50 50 Chapter Page IV. DISCUSSION . . . . . . . . . . . . . . . 6'! V. SUMMARY AND CONCLUSION . . . . . . . . . . . 75 BIBLIOGRAPHY . . . . . . . . . . . . . . . . . 77 iv Table LIST OF TABLES Partitioning of Rcoll as PL was varied in Four Dogs The Percentage Increase in Rcoll Calculated at Different Lobar Inflation Pressure (PL) Assuming the Resistance at PL = 25 cm H20 Equal 100% . . . . . . . . Segmental Airway Resistance R(Pbr-Ps) Values Compared to Total Collateral Resistance R(Pbr-PL) as PL Varied . Investigation of the Resistance From Multiple Sites of the Obstructed Segment . Volume of Gas Trapped by Lobes as Correlated to the Ratio of Segmental Airway Resistance to the Total Collateral Resistance During Both Inflation and Deflation . Page 37 46 49 51 52 LIST OF FIGURES Figure l. Diagrammatic illustration of method used to measure resistance to collateral flow . 2. Techniques for measuring the mechanics of collateral ventilation . 3. Circuit diagram illustrating the technique of resistance measurement used by Woolcock and Macklem . . . . 4. Diagrammatic illustration of the retrograde catheter in position . . . . 5. Diagrammatic representation of the equipment used to partition collateral resistance 6. Representative trace of the pressure gradient measurement between the bronchial catheter (Pbr) and the catheter in the main bronchus (PL), in the segment (P5) and in the extra- segmental area (PA) at PL = 2.5 cm H20 7. Subdivision of collateral resistance (Rcoll) plotted against lobe inflation pressure (PL) 8. Percentage increase in collateral resistance as a function of lobar inflation pressure (PL) obtained from individual dogs during inflation and deflation . . . 9. Subdivision of collateral resistance (Rcoll) expressed as percentage increase in resistance assumeing Rcoll = l00% at lobe inflation pressure (PL) = 25 cm H20, data was taken from Table 2 u . . . . . lO. Static pressure-volume curve obtained from one dog . vi Page ll 15 I9 30 33 4O 42 48 54 Figure ll. Subdivision of collateral resistance (Rcoll) expressed as a function of total lobe capacity (TLC) obtained from individual dogs 12. Subdivision of collateral resistance (Rcoll) expressed as percentage total lobe capacity (TLC . . . . . . . . . . l3. Diagram of an alveolar pore showing two radii of curvature which are affected by surface tension . . l4. Diagrammatic representation of the segmental catheters positions . . . . vii Page 56 6O 67 72 CHAPTER I INTRODUCTION AND LITERATURE REVIEW Historical Development The investigation of collateral ventilation started in 1883 when Kohn reported the existence of pores between the alveoli form- ing interalveolar communications. Before that the lung was believed to be a series of branches without intercommunications finally end- ing with separate alveolar sacs where gas exchange took place. The significance of these pores was ignored until Van Allen and co-workers (1930) reported that gas can transfer between lobules of the same lobe of dogs lung. However,the nature of these intercommunications was not known. Collateral ventilation was again ignored until Baarsma et. al. (l948) reported the existence of collateral ventilation in man. In their work the entire bronchus or the posterbasal or lateralbasal side branches of the bronchus of the lower lobe was obstructed by a catheter. The catheter had an inflatable cuff which could be filled with saline solution by means of a very thin rubber tube running through the catheter. The entrance of an airway was obstructed by the catheter when the cuff was inflated. The catheter was connected to a spirometer and a kymograph which recorded respiratory movements. A weight attached to the device I caused a negative pressure in the spirometer and the volume of the lobe connected to it. Air flowed into the negative pressure portion of the lobe and this collateral ventilation determined by an increase in the volume of the spirometer was recorded on the kymograph. The results of these experimetns indicated that collateral ventilation occurs in man only when a side branch of the main bronchus was obstructed. Upon obstruction of the main bronchus, collateral ventilation ceased and atelectasis developed. Possible Pathways for CollateraT'Ventilation Following the discovery of pores of Kohn scientists failed to agree on whether these pores were an artifact of fixation or the result of pathological changes such as emphysema. Macklin (1935) reported their existence in man, dog, cat, rabbit, guinea pig and rat. These pores or vents as he called them have a circular or oval shape and vary in size and number among mammalian species. Martin (1963) estimated there are about eight pores per alveolus in the dog lung. They seem to provide a means of equalizing alveolar pressure in the neighboring lung areas, and play a significant role in prevention of lobular atelactasis (Macklin, 1935). Lambert (1955) demonstrated other pathways for collateral ventilation, which she described as "tubular communica- tions lined with epithelial cells" connecting the terminal and respiratory bronchioles and the alveoli. These structures are found in rabbit, cat and man. Martin (1966) passed polyethylene spheres as large as 120 um i.d. between adjacent lung lobules and also injected India ink through bronchial branches of a lung lobe to outline the pathways for collateral flow. Serial sections were taken to trace the collateral pathways from a terminal bronchiole of one segment to terminal bronchiole of the adjacent segment. The results of these experiments convinced him of the presence of an interbronchial communications having a diameter between 200-300 um, lined with mixed cuboidal and flattened alveolar epithelium and connecting two respiratory bronchioles. Martin believed these respiratory bronchioles to be the main pathways for collateral Ventilation. In summary, three pathways for collateral ventilation have been described: (1) The pores of Kohn, having 3-13 pm i.d. connecting adjacent alveoli, (2) Lambert's canal, having a 30 um i.d., connecting respiratory bronchioles with alveoli, (3) Martin's channels having a diameter between 200-300 um connecting the bronchioles. Factors Affecting Collateral Ventilation Several physiological and pharmacological factors have been described which affect collateral ventilation. Hogg et a1. (1969) related the influence of volume history on collateral ventilation to the effect of surface tension which tends to narrow the collateral channels and the lung tissue elastic recoil which acts to make the collateral channels wider. The balance between those two forces determines the size of the collateral channels. Surface tension forces are greater when a given lung volume is approached during inflation after full deflation of the lung. Whereas the tissue forces are determined by lung volume regardless of the lung volume history. Because of the increased surface tension, the collateral channels are narrower during inflation and hence the resistance to flow is higher. Species differences also affect collateral ventilation. In anatomical studies by McLaughlin (1961), lungs of various mammals were grouped into three distinctive types. Type 1 represented by cow, sheep and pig, are extremely lobulated with thick pleura and interlobular septa. Type III which includes the horse have the same characteristics as group one except the lobulation is imperfectly developed. Type II includes the dog, cat and the monkey,and these are characterized by thin pleura and absence of septa. Human lungs are intermediate between the dog and the pig lung in their degree of lobulation (Woolcock and Macklem, 1971). The collateral transfer of air between lobules was demonstrated in many species lacking complete interlobular septa, however, it did not occur between adjacent lobes (Van Allen et al., 1930). Robinson and Sorenson (1978) showed that dogs have better collateral ventilation than horses, while Noolcock and Macklem (1971) showed that dogs have better collateral ventilation than man, and pig has no collateral ventilation. The observation of Lambert (1955) and Martin (1966) of the existence of interbronchioler and bronchio-alveolar communi- cations containing smooth muscles give the possibility of broncho- motor regulation of the collateral ventilation. It has been found that some drugs like epinephrine, isoproterenol and atropine sulfate increase collateral ventilation, while other drugs such as methacholine and histamine reduce it. Call et al. (1965); Chen et al. (1970) and Johnson and Lindskog (1971) . Alveolar gas composition also affects collateral venti- lation. Alveolar hypercarbia increases collateral ventilation, while alveolar ventilation with pure oxygen increases collateral resistance to flow and hence decreases collateral ventilation Chen et al. (1970); Johnson and Lindskog (1971) and Traystman et al. (1978) . Collateral ventilation increases in emphysema. Hogg et a1. (1969) found that the resistance of the collateral channels was higher in normal excised human lungs than in emphysematous lungs. They related this to emphysema which causes a distortion of the alveolar walls leading to the formation of fenestrae which decreases collateral resistance. Techniques Used to Study Collateral Ventilation Several different methods have been described to study collateral ventilation. A simple method was used by Van Allen et al. (1930) to show that air can transfer collaterally between .mom— .Pm um mac: soc; .zopw msu u o mmaoF Loan: «cu mo mcwcmao xmzcwm mg» um mczmmmcn n A4=Vopw u A42v>4_m u A44V>4._J IL .238an .25ch 238i 653n— mcammmi .8595. ‘- all) 30E .1.— 7222.3 263 2% _< 16 spaces. Since 0 can be determined and f is known, RC can be calculated. The time constant was measured at different fre- quencies and an average value was obtained. All methods for studying collateral ventilation and resistance rely on wedging a catheter in a fifth generation bronchus approximately 5 mm in diameter. Since collaterals originate at approximately the 17th generation, all measurements include a contribution by collateral pathways and a contribution by airways distal to the wedged catheter. There are however no extensive studies on the magni- tude of the contribution of these airways. Partitioning of Pulmonary Resistance The tracheobronchial system can be divided into two types of airways: (1) Conducting airways which include the trachea, bronchi and non-respiratory bronchioles. They occupy the 0 to 19th genera- tion. Trachea and bronchi differ from the non-respiratory bronchioles by possession of cartilaginous rings or plates. (2) Terminal respiratory units which include alveolar ducts and respiratory bronchioles. These lack cartilage and occupy the 20th to 27th generation. The total cross sectional area of the conducting airways does not increase significantly up to the 15th generation. In contrast, the total cross sectional area of the peripheral airways increases greatly beyond the 18th generation (Weibel and Gomez, 1962). 17 The contribution of peripheral to total pulmonary resistance has been investigated by Brown et al. (1969). Plastic beads of different sizes were used to artificially obstruct large and small airways of excised lung lobes of dog and pig. There was only a small increase in airway resistance when the lobes were infused with small beads, but a large increase in resistance when large beads were used. Since small beads obstruct small airways, the results indicate that the small airways contribute only a small portion of the total pulmonary resistance. Compliance becomes frequency dependent when there is a partial occlusion of the main bronchus in the dog because air cannot transfer between adjacent lobes. In contrast, air can transfer collaterally within the same lobe and it is therefore difficult to demonstrate frequency dependence of compliance in the dog when small beads obstructed the small airways. The pig showed frequency independence even when small beads were used indicating poor collateral ventilation. Frequency independence occured with complete airway obstruction with large beads in both species. Macklem and Mead (1967) developed the retrograde catheter technique to partition the lower airway resistance (Figure 4). The regrograde catheter is a polyethylene tube with a bell shape at one end. The catheter was positioned by inserting a large polyethylene catheter through the trachea until it was well wedged. A piano wire was then advanced through the wedged 18 Figure 4.--Diagrammatic illustration of the retrograde catheter in position. It extends from the bronchial Lumen, through the bronchial wall, parenchyma and pleural surface. From Macklem and Mead, 1967. 19 .9280 $200th . v 83E is 825m .285». Q J 20 catheter and out through the pleural surface. The large catheter was then removed and the end of the retrograde catheter was attached to the tracheal extension of the wire and by pulling the wire at the pleural surface, the retrograde catheter was pulled through the airways and the parenchyma until it was wedged in an airway. The disadvantages of the retrograde catheter is the distortion and trauma of the lung tissue through which it passes. The presence of the catheter could partially or totally immobilize the lung tissue for some distance in all directions and the consequences is that the flow past the catheter tip could be stopped. The bronchus in which the catheter is wedged would then act as an extension of the catheter and the pressure will be measured at the nearest branch where flow is occuring. This leads to an overestimation of the pressure drop between the catheter tip and the alveoli. The advantages of this method over the conventional method of bronchial pressure measurement is that the catheter does not totally block the airway where it is wedged, and by varying the size of the bell, the catheter could be wedged in different airway positions. The validity of these advantages is obviously dependent on the magnitude of the lung trauma. Once the catheter is wedged and the pressure is measured satisfactorily, the total pulmonary resistance could be parti- tioned into two components: (1) resistance between the top of the catheter and the alveoli or the peripheral resistance and the resistance between the retrograde catheter and (2) the 21 resistance between the regrograde catheter and the trachea or the central resistance assuming that the pressure in a single bronchus is representative of the other bronchi in the lung ofaisimilarsize. A slight modification of the retrograde catheter technique was used by Macklem et a1. (1969) in that a silk suture was tied to the catheter bell and extending from the trachea. The silk suture was used to move the catheter from the wedged position toward the trachea and the resistance was partitioned at different points. At the end of the experiment the dogs were killed and the lungs were removed and fixed in formalin and dissected to the points of measurements. -Airway diameter and generation were measured at each point. The resistance of lung tissue and all airways smaller than the one containing the catheter was defined as the peripheral resistance. central resistance was defined as the resistance of airways between the tip of the catheter and the trachea,and the total pulmonary resistance is the sum of both resistances. Resistance was plotted against the percentage V0 for three different airway diameters: Small airways (0-3.0 mm i.d.), medium airways (3-8 mm i.d.) and large airways (>8.0 mm i.d.). The effect of lung volume on airway resistance is greatest in the medium airways. Vagotomy decreased the resistance of all airways, but the greatest reduction in resistance occured in the medium size airways. The explanation for this related to the lack of sympathetic tone in the medium size airways which causes the vagal tone to produce its major effect on these airways. 22 Adrenergic mechanisms act selectively in the peripheral airways only and block the vagal tone at this level. Peripheral resist- ance was a small fraction of the total pulmonary resistance above 80% VC, however it becomes a significant part of the total resist- ance at a low lung volume, Macklem and Mead (1967). Hoppin et al. (1978) modified the retrograde catheter technique described earlier in that the gas pressure in the peripheral airspaces was directly measured with needles inserted through the pleural surface so that tissue resistance component was excluded. The experiment looked at the relationship of airway resistance to lung volume before and after vagotomy. The catheter was wedged in an airway 2-3 mm i.d. and peripheral resistance was calculated to be one third of the total resist- ance. The absolute values of resistance increased monotonically as the lung volume decreased, but peripheral resistance changed more than the central resistance as a function of change in lung volume. These authors could not confirm the earlier report that the greatest change in resistance was in medium size airways. They related the monotonic increase in resistance to the effect of smooth muscles on the airways at low lung volume. While vagotomy reduced the resistance, volume dependence remained. In summary, airways between 3-8 mm diameter comprise 50% of the total pulmonary resistance. Peripheral airways accounts for only 10% of the total resistance. All airway resistance appears to be volume dependent. 23 While several papers have compared central and peripheral resistance, few workers have compared airway and collateral resist- ance. Menkes et al. (1973) by using the retrograde catheter technique found that at PL = 5 cm H20 (equal to functional residual capacity - FRC -), the specific collateral resistance (Rcoll x VL) was ten times as great as the specific airway resistance (Raw x VL) and both resistances decreased rapidly as the lobe inflated to PL = 20 cm H20 where specific collateral resistance was equal to the specific airway resistance. This indicated that at high lung volumes, collateral pathways are more likely to be effective in providing ventilation than that at FRC. In a more recent study, Inners et al. (1979) found that both collateral and airway resistance decrease as VL increases. Assuming their isolated segment occupied 2-5% of lung volume they calculated that Rcoll was significantly greater than the Raw at FRC and this relationship did not change as VL increased from FRC to 80% of total Lobe capacity (TLC). Above 80% TLC the volume induced rate of decrease of Rcoll was greater than that of Raw. They concluded that collateral pathways are ineffective for the distribution of ventilation relative to airways between FRC and 80% TLC, however collateral pathways may be effective above 80% TLC. A direct method to study collateral resistance was provided by Hilpert in 1970 and was described earlier. Today this is the common method used to measure collateral resistance 24 and time constants. Catheters are wedged in 4-5 mm diameter airways approximately the fourth generation. If collateral pathways are respiratory bronchioles, they will begin at the 17th generation. When measuring Rcoll by Hilpert's method, resistance includes peripheral airways between the segment distal to the wedged catheter, collaterals, and extra segmental airways. Hogg et a1. (1969) partitioned the resistance as described earlier, while Menkes and Traystman (1977) partitioned the resistance from the PS-PL decay, where PS-PL is the driving pressure through the segmental and extrasegmental components. When flow was introduced into the segment via the wedged catheter, air leaked through the collateral channels and returned to the main bronchus. When flow was suddenly stopped, two or more patterns of pressure decay were observed. The first, a fast decay of pressure was followed by a slower decay. Since collat- erals are composed of population of airways having different resistances, the fast decay was due to a low resistive airways which could be the segmental airways, while other population of more resistive airways (true collaterals) caused the slower pressure decay. The second type of decay is a slow but uniform pressure decay caused mainly by high resistive collateral pathways. Most workers did not consider the fast decay of pressure and assumed that most of the resistance through the obstructed segment is due to collateral channels. The objective of this study was to determine the contribution of peripheral airways to 25 measurements of Rcoll in dog lungs. A catheter was inserted through the pleural surface in the isolated segment and another catheter was inserted into the extrasegmental area so that collateral resistance could be divided into three components. The segmental airway resistance R(Pbr-Ps) is defined as the resistance of airways between the wedged catheter and the catheter of the obstructed segment, R(Ps-PA) is the resistance across the boundary of the segment, R(PA-PL) is the extrasegmental resistance while R(Pbr-PL) is the total collateral resistance. Because collateral airway resistance is volume dependent, the parti- tioning of collateral resistance was performed at different lobar volumes during both inflation and deflation maneuvers. Since it is possible that collaterals are simply anastomising peripheral airways, then the volume dependency of collaterals and peripheral airways will be similar. CHAPTER II MATERIALS AND METHODS Surgical Preparation Fourteen dogs of mixed age, sex and breed were anesthe- tized with (10 mg/Kg) Sodium thiamylal (Surital, Park, Davis and Co., Detroit, Michigan). The dogs were killed by exanguination from the cut carotid artery. The chest was widely opened and the lungs removed. The lower left or right lobes was dissected free after the ligation of the pulmonary arteries and veins. The lobes were kept moist before and during the experiment by the applica- tion of saline to the pleural surface. The bronchus of a single lung lobe was connected to one arm of a three way connector (Figure 5). A second arm connected the lobe with a variable speed blower. The third arm allowed pas- sage of a catheter in order to isolate a segment of the lobe. The lobe was inflated using a rheostat controlled variable speed blower and any leaks were sealed with ligatures. If the leak could not be sealed, the lobe was excluded from measurements. Isolation of a Segment of Lose A double lumen polyethylene catheter was advanced into the lobe through the side arm of the three way connector while the 26 27 lobe was fully inflated. The outer lumen of the catheter (PE 350, 1.0. 3.99 nm) which had a bell shaped head (5 mn o.d.) was wedged in an airway in order to isolate a sublobar segment of the lung. The inner Lumen of the catheter (PE 60, 1.0. 0.76mm) was connected to a transducer (PM 131, Statham Hato Rey, PR) and an amplifier (PVD-22, Electronics for Medicine, White Plains, NY). In order to measure the lobe inflation pressure (PL) a needle was inserted into the main bronchus and attached to a similar catheter and transducer. Two polyethelyene catheters (PE 50, 1.0. 0.58 mm) were inserted 1-2 mm into the lung parenchyma through the pleural surface of the lobe. The first catheter was inserted into the isolated segment in order to measure the seg— mental pressure (Ps). The other catheter was inserted in the extrasegmental parenchyma to measure the alveolar pressure (PA). Leakage through the pleural surface due to the insertion of the catheters was sealed by using one drop of an adhesive (Eastman- 910) around the catheter tip. The PL catheter was connected to one side of a differen- tial transducer while the other side was Open to atmosphere. Pressure catheters (Pbr), (Ps), (PA) and a further (PL) were connected to a similar transducer by means of stopcocks, so that Pbr-PL, Pbr-Ps, and Pbr-PA could be measured (Figure 5). Pressures were displayed individually on an oscilloscope screen and recorded on the light sensitive paper of a multitrace recorder (VR-6 Electronics for Medicine, White Plains, NY). The pressure 28 transducer was calibrated daily against water manometer. The lobe was fully inflated while the double Lumen catheter was advanced to isolate the segment. The lobe was then deflated and the wedging of the catheter was checked by gently pulling on the catheter. Isolation of the segment was checked by recording Pbr-PL and PL during lobe inflation and deflation. If the catheter was wedged and the segment was isolated, Pbr-PL and PL were out of phase with Pbr-PL becoming negative at the beginning of inflation and returning to zero at the maximum inflation. During deflation Pbr-PL became positive with respect to PL at low lung volumes. Partitioning_9f Collateral Resistance Collateral resistance was measured at PL=25, 20, 15, 10, 5 and 2.5 cmHZO during both inflation and deflation of the lobe. During deflation maneuvers the lobe was inflated to 30 cmHZO (which is defined as PL = 30 cmH20) each time and then deflated to a desired PL. During inflation, the lobe was inflated to TLC and then deflated to zero PL before inflating to a desired PL. Catheter wedging was checked before each measurement. Under static conditions with no collateral flow and when the collateral pathways and airways are open, the pressure gradient Pbr-PL, Pbr-Ps, and Pbr-PA should be zero. Resistance was partitioned if these gradients were zero and if air could be freely withdrawn from the subpleural catheters. Air flow into the isolated segment came from a compressed air tank and was adjusted by a 29 .»_m>_uomammc mesmmmca copom>Pm may one mcammmca qucmsmmm msu .mczmmmca mecococn mzu .mcammmca xgmcospaamcmcu mg» men <¢ use ma .caa .4; .cmzopn a sum: umum_mcw mm one; och .cmumsouoc a ma umpmsnum mm 30pm .mocmumwmmc chmpoppou cowuwucmg o» now: acmEavzam as» mo cowumucmmmcamc ovumssmcmmwoul.m mczmwm 30 0 93mm ES. .3. 41' a --"’ -“—- \---------—--— c8388: :95 832m be $288”. 31 rotometer (Matheson No. 743l-T) to provide a pressure difference Pbr-PL = 1 cm H20 (Figure 6). The subdivision of collateral flow resistance (Rcoll) are calculated as the difference in pressure AP between the sites of pressure measurements divided by collateral flow (Vcoll) as recorded with the rotometer: AP Rcoll = Vcoll Three components were measured: Pbr-PL (1) Total collateral resistance R(Pbr - PL) =-7———-—— , Vcoll Pbr-Ps (2) Segmental airway resistance R(Pbr - P5) = -:---- . Vcoll (3) The resistance of the collaterals and the segmental Pbr-PA Vcoll airway resistance R(Pbr - PA) = Three other resistances were calculated: (1) The resistance across the boundary of the segment R(Ps - PA) = R(Pbr - PA) - R(Pbr - P5) (2) The extrasegmental resistance R(PA - PL) = R(Pbr - PL) - R(Pbr - PA) (3) The resistance across the segmental boundaries and the extrasegmental resistance R(Ps - PL). 32 .mucmsmcammms do mopem msu cmmzuma maopm>mu ocmwumcm mczmmmcn m .ucmEmmm swamFomw we» once cmozuocucw mp zap» cm 3 .oLmN mcm mucmwuocm mcammmca ago .3c_m Pmcmumppou o: m? mews“ ems: .o I So m.~ u on on Awumpcmmmcammuu.o mcamwm 33 1/ Ou> . <15 m 8:9... 5:58 mom u> ma .5... 49.5.. . O ....> . ouxeu nmun. 34 Lobar Pressure Volume Curves Pressure volume (P-V) curves of the lobes were obtained at the end of the experiment in four dogs by stepwise injection and removal of 50 ml increments of air using a 1500 ml syringe (Model 51500, Hamilton Co., Inc., Reno, NV). Injection of air was terminated when PL = 30 cm H20, usually 400-650 ml PL was recorded continuously on the multitrace recorder during injection and removal of air. Since Rcoll was measured at a variety of PL, the P-V curves permitted the description (If the resistance as a function of the total lobe capacity which is the volume obtained from the P-V curves plus the minimal volume. Measurement of Minimal Volume Lobe volume at PL = 0 cm H20 was measured by water displace- ment. Trapping gas by the lobe during the experiment was measured by subtracting the minimal volume of the lobe before the start of the experiment from its minimal volume at the end of the experiment. Measurement of the Segmental Volume At the end of the experiment, the boundaries of the isolated segment were marked on the pleural survace and the segment was injected with 2 ml barium contrast material. The lobe was inflated with air at PL = 30 cm H20 for a week. When the lobe was dry, the segment was dissected from the lobe by cutting along the boundaries on the pleural surface. The internal boundaries of the segment were defined by the barium contrast. The segment 35 volume was obtained by water displacement method after wrapping segments in plastic film. Mggsgrement of Pressgre gt Multiple Sites in the Segment The original hypothesis supposed that pressure is equal everywhere in the segment and the insertion of a catheter in any position in the segment is the representative of the segmental pressure. This assumption was checked in four dogs by insertion of three PE 50 polyethylene catheters (P51, P52, and Ps3) about 2 mm deep in different positions. Ps1 was positioned at the center of the segment, Ps2 at the boundaries, and Ps3 at the extrasegmental area. Pressure drop between the segmental airway catheter (Pbr) and that of segmental catheters were compared for each case. CHAPTER III RESULTS Fourteen dogs were used, six of which did not give complete data during inflation, deflation or both, so that only dogs which provided complete data were used in the present study. Most of the dogs which were not used had lungs that trap gas and made it impossible to measure resistance at low lung volumes. Leakage and atelactasis were other reasons for disregarding the data from other dogs. In measurements made on four dogs, the extrasegmental resistance R(PA-PL) was always a negligible value during inflation and always zero during deflation at all PL (Table 1). Because this finding agreed with previous findings, Hogg (1969), the measure- ment of this resistance was excluded from subsequent experiments. Only three resistance components were measured, the total collat- eral resistance R(Pbr-PL), the resistance of the segmental airways R(Pbr-Ps), and the resistance across the segmental boundaries together with the extrasegmental resistance R(Ps-PL). Effect of Inflation Pressure (PL) and velfime History on Lobe Collateral Resistance Collateral resistances R(Pbr-PL), R(Pbr-Ps) and R(Ps-PL) increased with decreasing PL. When Rcoll was plotted against PL, 36 37 oo.owo.o mo.uop. No.H¢o. mo.nop. oo.woo. eo.nmp. No.nmo. eo.Hm~. mm oo.ouo.o mo.HN—. No.H¢o. mo.nmp. oo.noo. eo.Hop. No.nmo. eo.nm—. om oo.o«o.o mo.wmp. No.Hmo. mo.ump. oo.Hoo. mo.HNN. No.emo. mo.n-. mp oo.owo.o mo.nmp. No.wmo. no.HmF. oo.Hoo. mo.nm~. mo.nmo. mo.«mm. o— oo.ono.o m_.Hmm. vo.nmo. mp.nmm. oo.noo. NF.H~¢. mo.HN_. NF.HN¢. m oo.o«o.o mm.umn. No.H¢~. mm.wnm. co.Hoo. ¢P.Hmm. eo.wmm. ¢¢.Hmm. m.~ A4muwuumammc cowucoa mocmumwmmc xmchm Popcmsmommcpxm «so mcwwapuxw mocmpmwmmc Pmcmpmppou page» asp vcm .mucmamwmmc xngpm Faucmsmmm mgu .mucmamwmmc chmpm—pou _muou may use A<¢1caavm can Ammucnmvm .A.aucamva .m=_m> mpnwmppmoc m mp A481 mm: .8 mm Ppoom co m:_:owp_ucma-u.P u.m

mzo; .mmmomcomu .. ma mmmmcucw A4¢1mavm mmwcmucaoa PmpcmEmmm as» mmocoa mucmumwmmc on“ new Ama-ca¢.m mucmumwmmc xngwm Faucmsmmm m..m-cnm.m mucmumwmmc chmpmppou Fmooh .A... oczmmmca copumpmcw one. omcwmmm nonpopa appoom. wocmumwmmc chmmeFou mo cowmw>wunsmuu.~ mczmw. Rcoll cmHZO/ml/sec 4O INFLATION '-°1 -—- R(Pbr-PL) 0.8‘ ""* R (PS-PL) 2'5 5 lb 115 2'0 .25 PL cmHZO DEF LATION 1.01 0.8' 0.6‘ 0.4‘ 0.2‘ Figure 7 41 .mmwcmvcson _mu=mEmom «so mmocum mucmomwmmc any n A4aumavm “mocmumwmwc >m3L_m Faucmsmmm u Amaucaavm "museumwmmc chmpmppou pmuou u 3.73%. .cozacme ea 832...... 22% 88 $3232., 8.: 8538 3.: es... -mmcn cowum—wcw cmaop mo :owpocsm a ma mocmumwmmc pmcmumppoo cw mmomcocw mmmpcmocmauu.m weaned 42 DEF LATION 800- , INFLATION 30G 70% ‘3' Deg ' 7004L 600 1“ HRflr’fi.’ 600. 500‘ E‘ MR(%'%) 500- ‘. ”“Rfs-L) 400‘ x 400- 300. zoo 100. = 25 5 |b 15 2D 5.5 25 8 8001 0: < 700. 600. 500« 400- 300. zoo. 100- 255 'b "5 2'0 2'5 ass P L Cm H20 5 '8'520215 Figure 8 'b 1? 26 23 43 INFLATION DEFLATION I400- \ D09 3 [400$ 1200-» \ “R(Pbr-P1.) 1200- 1000- \ :16??? 1000+ 800-» 800- 600- 400. 200- % 2'55 10 15 2'0 25 255 1'0 15 20 25 62 <1140m Dog 4 1400. 1200- ‘ 1200- 1000. \ 1000- 800- 600- 400- 200 25570 152025 255101552 PL cmHzO continuation of Figure 8 44 INFLATION 2800-( 1‘ 009 5 2300.1 2400- § “R(Pbr-P1.) 2400- 1 -----R(Pb,-Ps) 2000- 1 . 1‘ ”HRIPS 'PL) 2000 1600- 1. 1600- 1 1200- r,— . 255 10 15 2'0 2'5 800-1 400- DEF LATION 2800-1 2400-1 2000- l 6004 l 200- 800- 400- 255' PL cmHZO continuation of Figure 8 1'5 2'0 2'5 "/o A Rcoll 45 IN F LATION DEFLATION Dog 7 7001 “-‘RIPbr-PL) 600- ~--~R .2 mm muzuwcmme 25mm 252 now: mcwmcmgu A.21mavm mmwcmucaon paucwEmmm an» mmogom mocmumwmmc mgu can Amaucnavm magnuummc Amzcwm Panamammm .A.mucnavm mocmpmwmwc chmpmppoo Peach .N mpnmp Eoc¥ 20.2» me: name .ONIEo mm n A.¢. 223mmmca cowmemcw ago. an Roe. u Fpoum mewszmmm mucmumwmmc cw mmmmco:_ mmmucmucma mm cummmcaxm A_Fooav mocmpmwmmg chmomppoo mo cowmw>wunam1u.m mesmw. % A Boo" 1500-1 1400-1 1300- 1 100- 1000- 900~ 800- 700‘ 600- 500- 400. 300. 200- 100‘ 48 DE F LATION 2'55 10 15 2'0 25 2'55 10 1'5 2'0 2'5 PL CITlHZO Figure 9 49 TABLE 3.--Segmental airway resistance R(Pbr-Ps) values compared to the total collateral resistance R(Pbr-PL) as PL varied. (Mean 2 SE), n = 8 R Pbr-Ps PL R r-PL cmHZO INFLATION DEFLATION 2.5 0.3720.10 0.3520.08 5 0.2920.06 0.3020.05 10 0.2920.06 0.3020.05 15 0.2920.06 0.3020.05 20 0.2820.06 0.3120.06 25 0.2720.06 0.2820.07 50 Resistances are plotted as a function of volume and percentage TLC (Figure 12), inflation resistance was always less than deflation resistance below 75% TLC. Above 75% TLC resist- ance was similar on both inflation and deflation. Segment volume was obtained from five dogs and the mean 2 SE was (27.60 2 4.01) ml. Measurement of Pressure at Different Sites in the Segment The investigation of pressure at different sites in the segment have been done in four dogs. Results showed that pressure was not equal everywhere in the segment, but rather a clear con- centric shape of pressure was recognized. Resistance increased as the distance from the center of the segment towards the boundaries increased (Table 4). Lobar Volumes Lobe volume was measured at the beginning and the end of each experiment. Trapping gas as obtained by subtracting the volume of the lobe at the beginning of the experiment from its volume at the end of the experiment was correlated to the ratio between the segmental airway resistance R(Ps-PL) and the total collateral resistance R(Pbr-PL). Results (Table 5), show no significant correlation between trapping gas by the lobes and the ratio resistance. 51 Fo.neo. Fo.nmo. o.oHo.o po.H¢o. ~o.w¢o. Fo.HNo. Fo.ppo. Fo.H¢o. mN mo.nmo. po.Hmo. o.owo.o No.flmo. —o.nmo. —o.nmo. Fo.npo. —o.Hmo. om No.Hoo. Fo.pmo. o.ono.o menace. m04Hmo. mo.nmo. po.HFo. mo.Hwo. mp No.nmo. ~o.nvo. o.ono.o No.H~o. mp.no_. No.Hmo. Po.npo. op.no_. op ¢O.Hm—. No.Hmo. o.ono.o wo.nmp. Fo.H¢—. mo.nwo. No.Hmo. Fo.Hn_. m mo.Hm—. No.nno. o.oao.o mo.wm~. eo.nop. mo.nmo. No.nmo. mo.nmp. m.~ .mm2-222.m .Nma-aaa.2 ._m2-222.2 .52-Lna.m .mma-ana.m .Nma-252.2 .Pma-252.m .oa-222.m ONIEU uuzwpomqmmc mmuwm mommgzm Pmucmsmmmmcpxm new .mm_2mncaon .cmucmo as» on mucmsmgsmmme meammmca as“ 028 mm; new mma .pma .ucosmmm umuuzeumno ms» mo mmuwm mpawupze 2022 mocmpmwmmc 0;“ co :owummwpmm>c.11.¢ m4m

.cowumpmmu new cowumpccw span mcwgzu wocmumwmmc chmumF—oo Fmpou asp cu mace -om_mmg Angwm qucmsmmm mo ovum; any op umumpmccoo mm monop an umaamcu mam $0 mE=—o>-1.m m.m<~ 53 Figure 10.--Static pressure-volume curve obtained from one dog. Arrows show inflation and deflation maneuvers. PL = Lobe inflation pressure. 54 On aw. 9 9:9“. of .5 .2 ow M. .09 1w ewnloA v 55 .mmwcmuczon pavemEmmm mg» mmoeum mucmpmwmmc on» u .421mmvm ”magnumwmmg auzcwm Faucmsmmm u Ammucnmvm ”magnumwmwc Pmcmam__oo Page» u .4212navm .szcm 022 Fpoom :owumpmmu can Ppoom cowumpmcw weapo> mnop now; p< .mE:_o> mno_ 3o_ um F—oom cowum_$mc cusp mm0_ 933:. $3282 20329:: .320 3.6.5.6.: 59¢ 8538 8.5 3.538 mac— Pmuop co cowuoczm m we nmmmmcaxm Appoom. wocmpmwmmc Pmcmumppou we cowmw>wunam11.PP mc:m_. '4 1.4-1 ' 1 -——-1NFLAT10N 1.2. ' ----- ' DEFLATION 12.. 1.0- - Oool 1,0. .0- .6- .4- 8 2 £ 0 < i... E 1.4” o ‘ 12- '8 o... 1.0- a: .6- .6- .4- .4. .2- .2- 56 TLC ml 57 4.1 '—-° INFLATION . ., ----- DEFLAllON '3‘ Dog! Dog 2 8 ‘1 2 E 1- ‘ \ . O :13“ E 0 v v v v u a v r r i =5 .44 '41 o 0: Doc 3 0o. 4 .3 '4 ,3: 1 I -21 .24 .I - .1. 100 200 300400500600 100 200 300400500600 TLC ml continuation of Figure 11 R(Pbr'PS) Rcoll cmHZO/ml/sec -—-- INFLATION °---° DEF LATION Deal 58 I41 ’16 '5 J J l.0« 10'0 200300400500600 100200300400500600 0093 l .41 1.2- 100 200300 400500600 100 200 300400500 600 TLC ml continuation of Figure 11 R(Fg-PL) 59 .mmwcmuczon poucmEmmm on“ mmogom mocmpmwmmc 0;» u A421mavm "mocmumwmmc zmzcwm Fmpcmsmmm u Amaucnmvm ”wocmumwmmc chmmePoo Pope“ u A4212nmvm .AQ.H..xuwomamo maop Page“ mumpcmocmg mm ummmmcaxm AFPoomv mucmpmwmmc _mcmpmp_oo mo cowmw>wunzmuu.mp 023mm. cm HZO/mI/sec Rcoll 60 '41 7 R(PS'PL) °—-' INFLATION .3. ‘1 °"“'° DEFLATION 1.6l 1.4- 1.4- |.21 1.21 \ 1.0 1.0- .8- .8- .6- .6- .4- .4- .2- .2- 25 50 7'5 100 2'5 50 75 100 %TLC Figure 12 CHAPTER IV DISCUSSION The present study indicates that the extrasegmental resistance is of a negligible value. This result agrees with the findings of Hogg et a1. (1969) who reported that in excised human lungs resistance between extrasegmental alveoli and upper lobe airways was always too small to measure. Since resistance of intrasegmental airways has been known to provide the greatest site of resistance to flow, Woolcock and Macklem (1971) and Inners et al. (1969), it is clear that collateral pathways cause pressure to drop considerably so that very small or no pressure gradient can be measured between the extrasegmental alveoli and the upper lobe airways. Hogg et al. (1969) measured a considerable extra- segmental resistance in emphysematous lungs. Emphysema causes small airway obstruction accompanied by enlargement of pores due to the destruction of alveolar walls. Collateral resistance decreases as a result of emphysema and this plus small airway obstruction causes a great pressure gradient to develop between the extrasegmental and upperway catheters. Resistances R(Pbr-PL), R(Pbr-Ps) and R(Ps-PL) have been found to increase with decreasing PL and R(Pbr-Ps) accounts for 61 62 approximately 30% of R(Pbr-PL). Since the Pbr catheter was positioned in an approximately 5 mm diameter airway in the seg- ment, it would be equivalent to the peripheral airways obtained by Hoppin et al. (1978) and Macklem et al. (1967) and a combina- tioncfiiperipheral and central airways studied by Macklem et al. (1969). Hoppin et al. (1978) inserted a retrograde catheter in approximately 3 mm diameter airway to measure peripheral and central resistance as lung volume varied. Peripheral resistance was defined as the resistance of all airways below the position of the catheter while central resistance was the resistance of all airways upstream from the catheter position. Results showed that changes in peripheral airway resistance was greater than changes in central airway resistance as lung volume changed. There was threefold increase in peripheral resistance when per- centage VC changed from 50 to 20. These results are similar to the results obtained from the present study when R(Pbr-PL), R(Pbr-Ps) and R(Ps-PL) were expressed as percentage TLC indicat- ing that all airways investigated behave like peripheral airways. The present study showed that the percentage increase in R(Pbr-PL), R(Pbr-PS) and R(PS-PL) were similar as PL varied, however individual dogs showed considerable interanimal variation. The similarities of percentage increase in resistance was due to two main reasons: 63 (1) Since excised lobes were used, the effect of vagus nerve was abolished so that smooth muscles that lined airways would not have any influence on airway caliber. (2) Resistance measurements were made in similar struc- tures (peripheral airways) so that resistance changes are similar in all collateral components. This result contradicts the results of Inners et al. (1979) who reported that collateral and airway resistance changed with lung volume in similar fashion up to 80% TLC. Above 80%, collateral resistance decreased more than airway resistance. The results of Inners et a1. (1979) indicated that collateral pathways may be of some importance in ventilating the obstructed segment at high lung volumes, however at low lung volumes, this function may not be as important. In contrast, the results of the present study showed that the relative importance of airways and collaterals as pathways for ventilation does not differ as lung volume varies. R(Pbr-PL), R(Pbr-Ps) and R(Ps-PL) during inflation were higher than during deflation as PL varied. Pressure volume curves obtained from lobes at the end of experiments show that at a given PL the volume of air that can be introduced into the lobe during inflation is less than the volume of air that can be introduced during deflation. This difference in pressure volume hysteresis is due to the effect of surface tension which causes lobar airways to close at low lung volume. During inflation a 64 smaller lung volume results from a given PL because of higher surface forces. The smaller lung volume causes inflation collateral resistance to be greater than deflation collateral resistance. Graphs of Rcoll vs. lobar volume (Figure 11) show that inflation Rcoll is less than deflation Rcoll below 75% TLC. Robinson and Sorenson (1978) reported similar results. They found that inflation Rcoll is less than deflation Rcoll below 40% TLC. Results obtained from the present study were also in agreement with the results of Woolcock and Macklem (1971) who reported an inflation Rcoll less than deflation Rcoll in four dogs at a variety of percentage TLC. The results of this study are in contrast to those of Hogg et al. (1969) who found that inflation Rcoll is greater than deflation Rcoll. They suggested the influence of volume history on collateral channels was due to changes in surface tension and elastic recoil of lung tissue and that the resulting size of collateral channels depends on the balance between those two forces. Since tissue elasticity is the same during inflation and deflation above FRC at any given volume, surface forces would be the sole determinant of differences in Rcoll. At a given lung volume reached by inflation after a full deflation, surface tension would be greater than if this volume was reached by deflation after a full inflation. If increased surface forces, narrow collaterals, Rcoll will be greater during inflation. 65 The explanation provided by Hogg et a1. (1969) depends entirely on the geometry of collateral channels. If we assume that collateral channels are simply pores of Kohn, then their assump- tion may be in doubt as pointed out by Woolcock and Macklem (1971) who gave another explanation based on the existence of pores of Kohn as the primary collateral pathways. The effect of surface tension on the pores depends on the balance between the forces which tends to open them and that which tends to close them. Since the pore has two curvatures which are normal to each other (Figure 13), the effect of changing in surface tension would be dependent on the relative length of each radius of curvature (Menkes et al., 1971). If the radius of the alveolar wall is less than the radius of the pore's opening, then the increase in surface tension would increase the pore's opening according to Laplace theory which states that pressure due to surface tension is inversely proportional to the radius of the curvature of the surface. Increase in surface tension of a pore would tend to open it and hence decreases the resistance to flow through it. This would explain in part the volume history influence which has been observed in this study. An alternative explanation of the influence of lung volume history on Rcoll was given by Robinson and Sorenson (1978) who believed that collateral pathways behave like a bronchiole originating within the isolated segment and terminating in the 66 ._mm_ ..p0 00 .: .m0xc0z 502.. .Fpmz 0.0200 00 mzwcmc u mm .mcwc0ao 0.0500 mo 0:200; u _m .commc0p 0000230 ma 00000000 020 cows: 0czpm>cao mo 2.000 030 mcwzozm 0200 cmpo0>F0 :0 00 Emcmmwo11.m_ 0gsmw. 67 m. 22.2.2 68 adjacent lobular parenchyma. They used the relationship between bronchial diameter and lung volume proposed by Hughes et al. (1972) to explain the relationship between volume history and Rcoll. The relationship between bronchial diameter and lung volume depends on the relative magnitude of bronchial and lung pressure-volume hysteresis. If the lung hysteresis is greater than bronchial hysteresis, then bronchial volume is greater on inflation than on deflation and Rcoll would be less on infla- tion. Robinson and Sorenson (1978) inflated the lung after a full deflation, so that lung pressure-volume hysteresis increased and Rcoll became less on inflation compared to that on deflation. The relationship between airway diameter and lung volume pro- vided by Hughes et a1. (1972) suggests that collateral pathways hysteresis was less than lung hysteresis. Since the exact nature of collateral pathways is still unknown, the contradiction between the results provided by Woolcock and Macklem (1971), Robinson and Sorenson (1978) and the present study on one hand and Hogg et a1. (1969) is still an unresolved issue. A possible combination of the three earlier described collateral pathways could exist with each working at different levels of lung volume. Even though collateral channels are assumed to be the only sites for resistance to flow, Menkes et a1. (1971) tested the assumption that segmental airway resistance might contribute somewhat to the total collateral resistance. A catheter was 69 inserted in the obstructed segment so that the pressure drop from the wedging catheter (Ps) to the lobar bronchus catheter (Palv) can be compared with the pressure drop between the bronchial catheter and the catheter in the wedged segment. They reported ratios of pressure ranged between 2-16% which reflects the same amount of resistance provided that a constant flow is given. In the present study a higher resistance was obtained (30% 0f the total pulmonary resistance). Differences between the two results could be due to: (1) The number of animals used. While they reported results of only three dogs, data from eight dogs were used in the present study. (2) The segmental catheter which they used was closer to the wedged catheter. It has been demonstrated in the present study that resistance is not equal everywhere in the segment and the segmental catheter reflects the amount of airway resistance to the total collateral resistance. Segmental catheter measures alveolar or small airway pressure at a position in the isolated segment. Investigation of the pressure at different sites in the isolated segment show that resistance differs from one site to another. Hoppin et a1. (1978) confirmed this result. They inserted two parenchymal needles to measure the peripheral resistance. They found that values obtained from one site was on the average two times that obtained from the other site. 70 Anatomy of the isolated segment shows that the segment consists of a series of branches which branch into smaller and smaller airways ending with alveolar ducts and alveoli. Consider- ing this anatomy we can see that the segment is not simply behav- ing like a balloon where pressure is equal everywhere, but rather a series of branches lined with smooth muscles and other support- ing elements. Since collateral resistance has not been partitioned before, workers supposed that collateral pathways provided the major site for collateral resistance. In the present study it has been found that the position of the (P5) catheter reflects the amount of pressure it measures (Figure 14). Segmental catheter (P51) could be in a position closer to the wedged catheter (Pbr) so that the pressure gradient between those two catheters would be less than the pressure gradient of another catheter (P52) which was located at a position further away from the wedged catheter. At a given flow the resistance of R(Pbr-P52) would be higher than R(Pbr-P51) and if another catheter (Ps3) was placed extrasegmently then resistance between the wedged catheter and this catheter would be even higher. R(Pbr-Ps - R(Pbr-P52) and R(Pbr-R52) - R(Pbr-P51) give 3) us an indication that resistance increases as we approach the boundaries of the segment, but it is not the collateral pathways which provide the major site for collateral resistance; peripheral airways might be as important as collaterals. 71 .00000300000 000005000 00 0000 0:0 00 00030005 00300000 u 000 ”0000000300 000205 1000 000 :0 0020000000 00000000 u ~00 ”0005000 0:0 00 000200 0:0 :0 0000000000 00002000 ~00 .000000000 000000000 000205000 0:0 00 00000000000000 00005500m00o11.¢_ 00:00. ”—-- § 72 Figure 14 73 Segment volume (mean 2 SE) was measured using the method described earlier. The average segment volume is 27.6 2 1.4 ml. The isolated segment size for dog lobes was estimated by Woolcock and Macklem (1971) using a radiographic technique to range between 8 and 140 ml with an average 52.4 i 3.5 m1. Another method was described by Menkes et al. (1973) where 1 - 3 m1 of a mixture of tantalum particles were used to outline the segment. Lobes then were dried at PL = 30 cm H20 for 8 - 10 days. Lobes were then dissected and segment volume was obtained by dry displacement technique. Their results ranged from 8 to 37 ml with an average 17 i 2.4 ml. Robinson and Sorenson (1978) used the same tech- nique described by Menkes et al. (1973) to introduce 3 - 5 ml of contrast media. They reported a mean 24.8 i 3.9 ml for dog lobes. The results obtained from the present study are in agreement with the findings of Robinson and Sorenson (1978), but deviated from the results of Menkes et al. (1973) and Woolcock and Macklem (1971). It is believed that the segment volume found in the present study was fairly accurate for two reasons. First, the segment boundaries were outlined with ink before injection of barium to know whether it stays in the segment or distributed in the extrasegmental area. Second, only a small volume of barium was used to avoid distribu- tion of barium outside the segment. The previous requirements must be met before dissection of lobes were made. Lobes which did not meet those requirements were excluded from measurements. 74 In summary, results showed that R(Pbr-Ps) and R(Ps-PL) are volume dependent. The behavior of R(Pbr-PL), R(Pbr-PS) and R(Ps-PL) as a function of PL indicates that resistance measure- ments have been made in airways of similar structures (peripheral airways). The relative importance of collaterals and peripheral airways as pathways for ventilation does not vary with lobe volume. CHAPTER V SUMMARY AND CONCLUSION The results of the present study indicate that: (l) The extrasegmental resistance R(PA-PL) is of a negligible value. (2) Total collateral resistance R(Pbr-PL), segmental air- way resistance R(Pbr-Ps) and the resistance of the collateral pathways R(Ps-PL) increase with decreasing PL. (3) At a given PL, collateral resistance is greater during inflation than that during deflation. (4) When collateral resistance was plotted as a function of total lobe capacity (TLC), inflation resistance was less than deflation resistance below 75% TLC. (5) The percentage increase in resistance with decreasing PL is the same in all collateral subdivisions. (6) R(Pbr-PS) is approximately 30% of R(Pbr-PL). (7) The mean segmental volume is 27.6 2 4.01 (SE) ml. (8) Gas trapping by lobes averages 32.38 2 6.3 (SE) ml. (9) Pressure at different sites in the isolated segment of the lobe is not equal but rather a concentric shape of resist- ance existed indicated that one (Ps) may not be representative of the whole pressure in the segment. 75 BIBLIOGRAPHY 76 BIBLIOGRAPHY Baarsma, P.R.; Dirken, M.N.J.; and Huizinga, E. "Collateral Ventilation in Man." J. Thorac. Surg., 17:252-263. 1948. Brown, R.; Woolcock, A.J.; Vincent, N.J.; and Macklem, P.T. "Physiological Effects of Experimental Airway Obstruction with Beads." J. Appl. Physiol., 27:328-335. 1969. Call, E.P.; Lindskog, 0.; and Liebow, A. "Some Physiological and Pharmacological Aspects of Collateral Ventilation." J. Thorac. Cardiovasc. Surg., 49:1015-1025, 1965. Chen, C.; Sealy, W.C.; and Seaber, A. "The Dynamic Nature of Collateral Ventilation." J. Thorac. Cardiovasc. Surg., 59:518-529, 1970. Hilpert, P. Collaterale Ventilation Habilitationschrift, Ans der Medizinischen, Thesis, Tuebingen Universitatsklinik, 1970. Hogg, J.C.; Macklem, P.T.; and Thurlbeck, W.M. "The resistance of Collateral Channels in Excised Human Lungs." J. Clin. Invest., 48:421-431. 1969. Hoppin, F.G., Jr.; Green, M.; and Morgan, M.S. "Relationship of Central and Peripheral Airway Resistance to Lung Volume in Dogs." J. Appl. Physiol. Respjrat. Environ. Exercise Physiol., 44(5):728—737, 1978. Hughes, J.M.B.; Hoppin, F,G.; and Mead, J. “Effect of Lung Inflation on Bronchial Length and Diameter in Excised Lungs." J._Appl. Physiol., 32:25-35, 1972. Inners, C.R.; Terry, P.B.; Traystman, R.J.; and Menkes, H.A. "Effects of Lung Volume on Collateral and Airways Resistance in Man." J. Appl. Physiol. Respirat. Environ. Exercise Physiol., 46(11167-73, 1969. Johnson, R. and Lindskog, G. "Further Studies on Factors Influ- encing Collateral Ventilation." J. Thorac. Cardiovasc. Surg., 62:321-329. 1971. 77 78 Lambert, M.W. "Accessory Bronchiole-alveaolar Communication." J. Pathol. Bacteriol., 70:3110314, 1955. Macklem, P.T. and Mead, J. "Resistance of Central and Peripheral Airways as Measured by a Retrograde Catheter." J. Appl. Physiol., 22:395-401. 1967. Macklem, P.T.; Woolcock, A.J.; Hogg, J.C.; Nadel, J.A.; and Wilson, N.J. ”Partitioning of Pulmonary Resistance in the Dog.“ J. Appl. Physiol., 26(6):798-805, 1969. Macklin, C.G. "Pulmonary Alreolar Vents." J. Anat., 69:188- 191, 1935. Martin, J.B. "Respiratory Bronchioles as the Pathway for Collateral Ventilation." J. Appl. Physiol., 21:1443- 1447, 1966. Martin, H.B. "The Effect of Aging on the Alveolar Pores of Kohn in the Dog." Am. Rev. Respir. Dis., 88:773-778, 1963. McLaughlin, R.F.; Tyler, W.S.; and Canada, R.0. "A Study of the Subgross Pulmonary Anatomy in Various Mammals." Am. J. Anat., 108:149-165, 1961. Menkes, H.; Gardiner, A.; Gamsu, 0.; Lempert, J.; and Macklem, P.T. "Influence of Surface Forces on Collateral Ventila- tion.“ J. Appl. Physiol., 31:544-549, 1971. Menkes, 0.; Lindsay, D.; Gamsu, 0.; Wood, L.; Muir, A.; and Macklem, P.T. "Measurements of Sublobular Lung Volume and Collateral Flow Resistance in Dogs." J. Appl. Physiol., 35:917-921, 1973. Menkes, H.A. and Traystman, R.J. "Collateral Ventilation." Am. Rev. Resp. Dis., 116:287-309, 1977. Robinson, N.E. and Sorenson, P.R. "Collateral Flow Resistance and Time Constants in Dogs and Horse Lungs." J. Appl. Physiol. Respirat. Environ. Exercise Physiol., 44:63- 68,1978. Traystman, R.J.; Terry, P.B.; and Menkes, H.A. "Carbon Dioxide - A Major Determinant of Collateral Ventilation." J. A 1. Physiol. Respirat. Environ. Exercise Physiol., 4511): 69-74, 1978. 79 VanAllen, C.M.; Lindskog, G.E.; and Richter, H.G. "Gaseous Interchange Between Adjacent Lung Lobules." Yale J. Biol. Med., 2:297-300, 1930. Weibel, E.R. and Gomez, D.M. "Architecture of the Human Lung." Science, 137:577-585, 1962. Woolcock, A.J. and Macklem, P.T. "Mechanical Factors Influencing Collateral Ventilation in Human, Dog and Pig Lungs." J.AAppl. Physiol., 30:99-115, 1971. 111' MICHIGAN STATE IIIIIIIIIIIIIIIIIIIIIIIIIIIIII 3129310 63 UNIV. LIBRAR ES 11111111111111