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J Thorac Cardiovasc Surg 1996;112:85-93
© 1996 Mosby, Inc.
CARDIAC AND PULMONARY REPLACEMENT |
Supported by National Institutes of Health grant 1 R01 HL41281.
Received for publication Oct. 10, 1995 Accepted for publication Nov. 21, 1995. Address for reprints: G. Alexander Patterson, MD, Professor of Surgery, Division of Cardiothoracic Surgery, Suite 3108, Queeny Tower, One Barnes Hospital Plaza, St. Louis, MO 63110.
Abstract
The degree of lung allograft inflation during harvest and storage may affect posttransplantation function. High volume ventilation causes pulmonary vascular injury and increased pulmonary capillary permeability. However, the effect of lung inflation on pulmonary capillary permeability after hypothermic flush and storage is unknown. The current study was designed to examine the effects of hyperinflation and hypoinflation during preservation on pulmonary vascular permeability. Methods: An isolated, ex vivo rabbit lung gravimetric model without the confounding effects of reperfusion was used to determine post pulmonary capillary filtration coefficient (Kf). New Zealand White rabbits (2.75 to 3.15 kg) were intubated and the lungs ventilated with room air (tidal volume 25 ml). After sternotomy and heparinization, the pulmonary artery was flushed with low potassium dextran–1% glucose solution (200 ml). The heart-lung block was then excised. Two studies were conducted. For measurement of changes in airway pressure and lung volume during preservation, lungs were inflated to one of four storage volumes (12, 25, 40, 55 ml) with room air, 100% O2, or 100% N2 and stored at 10° C in a sealed container filled with saline solution. During preservation, lung volume and airway pressure were measured at 3, 6, 12, and 24 hours. In the Kf study, lungs were inflated with 100% O2, 50% O2 (with 50% N2), or room air and preserved. After 24 hours of preservation at 10° C, the heart-lung block was suspended from a strain-gauge force transducer and the lungs were ventilated with room air. The pulmonary artery was connected to a reservoir of hetastarch solution (6% hetastarch with 0.9% saline solution). Lung weight gain, airway pressure, pulmonary artery pressure, and left atrial pressure were measured continuously. After a brief flush with hetastarch solution, the reservoir was then elevated to achieve 1.0 to 1.5 mm Hg increments in pulmonary artery pressure. Results: The slope of subsequent steady-state lung weight gain was used to determine the Kf. The current study demonstrated the following: (1) changes in lung volume and airway pressure during storage increased with intraalveolar O2 concentration, (2) irrespective of inflation, fraction of inspired oxygen, hyperinflation during lung preservation increased the Kf in a volume-dependent fashion; (3) Kf was increased in lungs stored hypoinflated with room air; and (4) at any inflation volume, the Kf was significantly increased with 100% O2inflation after 24 hours of preservation. Conclusion: These results suggest that storage at high lung volume or high inspired oxygen fraction increases pulmonary capillary permeability. (J THORAC CARDIOVASC SURG 1996;112:85-93)
The optimum state of lung inflation during preservation has been a subject of considerable interest for many years. One study found that canine lungs stored in a deflated state for more than 1 hour at normothermia could not support life.
1 That same study demonstrated that static inflation during ischemia maintained canine lung function longer than ventilation. In the canine lung, improved tolerance to normothermic ischemia was shown by maintaining lung volume above functional residual capacity. 2 Locke and colleagues 3 have shown that preservation after pulmonary artery flushing with Euro-Collins solution and lung inflation is superior to the preservation provided by topical cooling alone after absorption atelectasis of the lung. These studies suggest that atelectasis of the lung should be avoided during storage.
In most clinical and experimental lung transplant programs, the donor lung is inflated during storage. However, the appropriate inflation volume of the donor lung during storage is not known. With an in situ hilar occlusion model, Fonkalsrud and associates 4 evaluated the function of the ischemic expanded dog lung. They demonstrated that static expansion of dog lungs for 8 hours at 10 cm H2O airway pressure resulted in superior function in comparison with that observed in lungs stored at 25 cm H2O airway pressure. In contrast, we 5 have previously demonstrated in a canine single-lung transplant model that static hyperinflation of donor lungs at 30 cm H2O airway pressure resulted in superior gas exchange function after 30 hours of cold storage.
In physiologic studies with ventilated lungs, it has been reported that, at high lung volumes, capillary permeability is increased and pulmonary edema tends to occur. 6-10 Parker and associates 11 reported that pulmonary vascular permeability increased with peak airway pressure in isolated and perfused dog lungs. Furthermore, Hernandez and colleagues 12 showed in rabbit lungs that volume distension by mechanical ventilation produces microvascular damage that increases the pulmonary vascular filtration coefficient (Kf). Although these experimental data indicate that high-volume ventilation will cause pulmonary vascular injury, there has been no consensus in clinical and experimental lung transplantation concerning the efficacy of storing lungs in a hyperinflated state.
We have previously used an isolated rabbit lung model to estimate the effect of ischemic storage condition on Kf, independent from the effect of reperfusion. 13 This model was used in the present study to examine two important issues. First, we studied the effects of inflation volume and inflation O2 concentration on ischemic time-dependent decreases in lung volume and airway pressure during storage. Second, we investigated the effects of a variety of inflation volumes and intra-alveolar O2 concentrations on Kf after 24 hours of preservation.
Material and methods
Study groups.
In the first part of the study, the effects of hypoinflation (lung inflation volume [LIV] 12 ml), normoinflation (LIV 25 ml), and hyperinflation (LIV 40 and 55 ml) on time-dependent changes in airway pressure and lung volume were studied. Room air, 100% O2, and 100% N2 were used in the evaluation of the effect of intra-alveolar O2 concentration on changes in airway pressure and lung volume during 24 hours of preservation.
In the second part of the study, the effects of several inflation volumes (12, 25, 40, and 55 ml) on Kf were evaluated after 24-hour preservation. In this second part of the study, the lungs were inflated with 100% O2, 50% O2 (with 50% N2), or room air and preserved for 24 hours at 10° C. Because our previous study demonstrated that the Kf of lungs inflated with 100% N2 was extremely high after 24-hour preservation, 13 100% N2 was not used in the current Kf study.
Excision and preparation of preserved lungs.
The preparation of the heart-lung block has been previously described. 14,15 In brief, New Zealand White rabbits, free of respiratory infections and weighing 2.75 to 3.15 kg, were premedicated with subcutaneous atropine sulfate (0.25 mg/kg), ketamine hydrochloride (35 mg/kg), and acepromazine maleate (0.6 mg/kg) and anesthetized with intravenous sodium thiopental (25 mg/kg). Minimal supplementary doses of thiopental were given when required. The animals were heparinized (700 IU/kg). An endotracheal tube was introduced through a cervical tracheostomy and the animals connected to a mechanical ventilator (model 671, Harvard Apparatus Co., Millis, Mass.: tidal volume 25 ml; rate, 30 breaths/min; positive end-expiratory pressure, 0.5 cm H2O). After median sternotomy, the bilateral superior venae cavae, the inferior vena cava, the ascending aorta, and the main pulmonary artery were dissected free and loosely encircled with individual ligatures. A 2.2 mm diameter tube (No. K50L, Baxter Healthcare Co., Valencia, Calif.) was introduced into the main pulmonary artery through the right ventricular outflow tract and secured in place. Cardiac inflow occlusion was accomplished by ligation of all three venae cavae and the pulmonary artery was ligated around the cannula. The left atrial appendage was excised, and the pulmonary artery flushed with low potassium dextran solution containing 1% glucose (LPDG). 16 All lungs were flushed with 200 ml LPDG by gravity from a height of 60 cm above the chest. After completion of the flush, a 19-gauge tube (model 88ID9F18, Terumo, Tokyo, Japan) was inserted in the left atrium through the opening of the excised atrial appendage, and the heart, lungs, and esophagus were excised en bloc. During this dissection, utmost care was taken to prevent lung injury from atelectasis, disruption of the lung surface, or any manipulation of lung tissue. The lungs were continuously ventilated during this procedure. The tracheal tube was clamped with the lung inflated at end-tidal volume. The heart-lung block was then completely immersed in 10° C saline solution. All lungs were kept at 10° C for 24 hours.
Animals were cared for in accordance with the "Principles of Laboratory Animal Care" formulated by the National Society for Medical Research and the "Guide for the Care and Use of Laboratory Animals" prepared by the Institute of Laboratory Animal Resources and published by the National Institutes of Health (NIH Publication No. 86-23, revised 1985).
Estimate of time course of airway pressure and lung volume during lung preservation.
In the present study, all lungs were ventilated at 25 ml tidal volume with room air until the end of the LPDG flush. After clamping of the tracheal tube, all excised heart-lung blocks except those in the 12 ml inflation group were placed in a watertight Plexiglas acrylic container that was filled with 10° C saline solution (Fig. 1). The remaining air in the container and a calibrated tube (Bentley ByPass tubing, 1/8 x 1/32 inch, Bentley, Irvine, Calif.) were then flushed out with 10° C saline solution. In the 40 or 50 ml inflation volume groups, 15 ml or 30 ml of gas (room air, 100% N2, or 100% O2) was added to the lungs by a syringe (1 ml/sec). Increased lung volume as a result of gas inflation was measured by displaced volume of saline solution from the container. In the 12 ml inflation volume group, the tidal volume of the ventilator was decreased to 12 ml after LPDG flush, and then the lungs were ventilated 10 times before clamping of the tracheal tube. The heart-lung blocks in this group were mounted in the container in the same manner as in the other groups. These containers were kept in a refrigerator at 10° C for 24 hours. During storage, airway pressures were measured (Accudata 143, Honeywell, Denver, Colo.) and recorded (model 2600, Gould, Cleveland, Ohio) 3, 6, 12, and 24 hours after the inflow occlusion. As shown in Fig. 1, volume changes in the lungs were measured at the same time by the saline solution displacement method with use of the calibrated tube.
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Calculation of original lung volume.
Original lung volume was defined as the lung volume just before storage. The original lung volume (OLV) was calculated as OLV = CV - RSV - HBV + TDV, where CV is the container volume, RSV is the volume of saline solution remaining in the container after preservation, HBV is the volume of the heart block, and TDV is total decreased volume of the lungs. Volume of the heart block was measured by the saline solution displacement method after removal of the lungs. In the 12 and 25 ml inflation groups, original lung volume was used to calculate a percent change of volume in each group. In the 40 and 55 ml inflation volume groups, a calculated volume (original lung volume minus displaced volume) was used in estimation of the percent change.
Estimation of initial peak airway pressure and Kf.
The assessment technique used to estimate the Kf was the same for all groups. After completion of each preservation period, a glass rod was inserted through the esophagus. With this glass rod, the heart-lung block was suspended from a strain-gauge force transducer (model FT03, Grass Instruments, Quincy, Mass.) and placed within a Plexiglas acrylic box that was maintained at a constant temperature (37° C) and humidified. The strain-gauge force transducer was attached to a recorder (model 2600, Gould) that was calibrated full scale from 0 to 10 gm via a bridge amplifier (Accudata 143, Honeywell, Denver, Colo.). The lungs were ventilated with room air (tidal volume 25 ml; rate, 30 breaths/min; positive end-expiratory pressure, 0.5 cm H2O). Peak airway pressure 30 seconds after the start of reventilation was measured as initial peak airway pressure (IAP). After an assessment of IAP, the lungs were flushed with 30 ml of room-temperature hetastarch solution (6% hetastarch solution with 0.9% NaCl, DuPont Pharmaceutical, Wilmington, Del.) in which the pH was adjusted to between 7.35 and 7.45 before each experiment. Flushing pressure was kept 1 to 2 mm Hg higher than the airway pressure. This flushing was completed within 5 minutes. After flushing, the left atrial cannula was sealed, and the pulmonary arterial cannula was attached to a suspended reservoir of hetastarch solution. Changes in pulmonary artery pressure (Ppa), left atrial pressure (Pla), airway pressure, and weight of the preparation were continuously measured (Accudata 143, Honeywell) and recorded (model 2600, Gould) during the assessment. Before measurement of the Kf, the lungs were hyperinflated twice to remove any areas of atelectasis. Thus peak airway pressure of all suspended lungs was decreased to less than 11 cm H2O at the beginning of Kf assessment.
Assessment.
Increases in Ppa and resulting lung weight were accomplished by elevation of the reservoir. Ppa was raised from airway pressure (10 to 11 cm H2O) to 17 cm H2O in 1.0 to 1.5 cm H2O increments at 8-minute intervals. After each elevation of the reservoir, rapid weight gain was observed within the first 2 minutes. This rapid weight gain was likely the result of increased endovascular volume caused by the increased hydrostatic pressure. This phase was followed by a slower rate of weight gain, which we interpreted as filtration of fluid out of the microvasculature into the lung interstitium. Pla increased to the same level as Ppa (Ppa = Pla = pulmonary capillary pressure) during the first 2 to 5 minutes, and after this period the rate of weight gain became stable. The rate of weight gain during the last 3 minutes of each 8-minute interval was plotted against pressure to determine the Kf.
Calculation of Kf.
The rate of weight gain was plotted as a function of pulmonary capillary pressure. A two-variable linear regression was used to obtain the Kf as the slope of the line relating the weight gain rate and pulmonary capillary pressure. At Ppa higher than 15 cm H2O, acceleration in the rate of weight gain was sometimes observed and steady state of Pla (Ppa = Pla) could not be achieved. We excluded these points when a curve became nonlinear (correlation coefficient [r2] < 0.96). Under these conditions, the initial three to five points were used to calculate the Kf in each case. The Kf was expressed as grams per minute per centimeter of water per 100 gm wet lung weight.
Wet lung weight (WLW) was calculated as WLW = TW – RW, where TW is total weight of the preparation before assessment and RW is weight of the remaining tissue after the lungs were removed from the preparation after assessment.
Statistical methods.
The results are presented as the mean plus or minus the standard error of the mean. Statistical analysis was done by analysis of variance (factorial or repeated measures). Statistical significance was accepted at the 95% confidence level, p < 0.05.
Results
Effect of inflation volume and intraalveolar O2 concentration on change in airway pressure during 24-hour preservation.
Table I shows the change in airway pressure in all groups. Inflation from 25 ml to 40 or 55 ml with room air, 100% O2, and 100% N2 increased airway pressure significantly (p < 0.001). In all groups, higher inflation volume caused higher airway pressure during 24-hour preservation. The airway pressure of the normal and hyperinflated lungs decreased almost at a parallel rate for 24 hours in the groups with identical fraction of inspired O2 values. In the hypoinflated lungs, airway pressure was significantly (p < 0.001) lower than that in the normal inflation groups before preservation. In lungs hypoinflated with 100% O2, the airway pressure decreased at a rate parallel to that in the normal inflated lung. On the other hand, in lungs hypoinflated with 100% N2, there was no change in airway pressure during 24 hours of preservation. At any inflation volume, 100% O2 inflation decreased airway pressure more rapidly than 100% N2 inflation (p < 0.001) during 24-hour preservation. In all groups, the airway pressure decreased to less than 8 mm Hg within the first 12 hours.
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shows the changes in lung volume during 24 hours of preservation. There was no significant difference in decreased volume between normally inflated (25 ml) and mildly hyperinflated (40 ml) lungs, irrespective of differences in inflation gas. In the 100% O2 inflation group, volume decrease in 55 ml inflated lungs was significantly larger (p < 0.01) than that in the other groups. Volume decreases in lungs inflated with 12 ml room air or 100% N2 were significantly smaller than those in the normoinflated and hyperinflated lungs (p < 0.05). At each inflation volume, lung volume decreased more rapidly (p < 0.001) with the increase in intraalveolar O2 concentrations (100% N2 < room air < 100% O2).
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). In the lungs inflated with 50% O2, the IAPs of the normal and hypoinflation groups were significantly higher than that of the hyperinflation group (p < 0.05 and p < 0.01, respectively). The IAPs of normal and hypoinflated lungs with 100% O2 were also higher than that of the hyperinflation group (p < 0.05).
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and Fig. 3. Hyperinflation (LIV 40 and 55 ml) increased Kf with inflation volume (p < 0.01 and p < 0.001, respectively). Hypoinflation also increased the Kf significantly (p < 0.01).
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). Furthermore, Kf of hyperinflated lungs (40 and 55 ml) with 50% O2 was significantly lower than that observed in lungs inflated with room air (p < 0.05). In lungs hypoinflated with 50% O2 there was no increase in Kf.
Inflation with 100% O2.
In this group, Kf of severely hyperinflated lungs was significantly higher than that of normoinflated and hypoinflated lungs (Table IV). Interestingly, Kf of the lungs inflated with 100% O2 was significantly higher than that of lungs inflated with room air and 50% O2 at any inflation volume.
Discussion
Although several groups have indicated that the duration of tolerable lung ischemia may be prolonged if the lungs remained ventilated or inflated during the ischemic interval, 1-5 in those studies, the effects of static inflation volume and intraalveolar O2 concentration on the decrease in lung volume and airway pressure during storage were not investigated. The present study reveals the effects of changes in lung volume and airway pressure during storage for 24 hours.
In the current study, we observed the change in lung volume by use of a saline solution displacement method. Hence the change in lung volume included the volume changes in lung parenchyma, airway, and intravascular volume. Because the cannulas placed in the pulmonary artery and the left atrium were closed during storage, change in intravascular volume was relatively small. It is likely that decreases in the lung volume in the current study mainly reflected the change in lung parenchyma and airway volume.
One of the mechanisms that causes a decrease in lung airway volume is diffusion of O2, N2, and CO2 into the immersing solution through the pleura. Faridy and Naimark 17 demonstrated that intra-alveolar O2 diffused easily to the extrapulmonary space through the pleura. The current study demonstrated that, by increasing the intraalveolar O2 concentration, lung volume and airway pressure decreased more rapidly during preservation. Volume decrease in the lungs inflated with 100% N2 was minimal. It is well known that O2 is almost twice as water soluble as N2, and that the dissolution rate increases with O2 tension. Although CO2 is the most water-soluble gas, its concentration in the airway is very low. Therefore, in this model, we speculate that the increase intraalveolar O2 concentration may have caused the increase in the dissolution rate of O2 and subsequent decrease of lung volume.
During the assessment, all lungs were ventilated at the same tidal volume of 25 ml. Therefore peak inspiratory pressure can be used to infer airway resistance. We found that the IAP of hyperinflated lungs was lower than that of normal and hypoinflated lungs in the room air–inflated group. Furthermore, in the 50% and 100% O2 inflation groups, which lost volume during storage, IAP of the normoinflated lung and of the hypoinflated lung was higher than IAP of the hyperinflated lung. It has been demonstrated that distention of the lung enhances the release of surfactant and that this release is a metabolically active process. 18 Also, decreased intraairway volume may cause microatelectasis, even though tracheal pressure remains positive. This may further explain why higher IAP was observed in the hypoinflated groups.
In the current study, Kf of lungs inflated with room air increased with lung inflation volume before storage. Increase in intraalveolar O2 concentration to 50% reduced the detrimental effect of room air hyperinflation on Kf, although severe hyperinflation with 50% O2 (LIV 55 ml) still increased Kf significantly. An increase in airway O2 concentration to 50% reduced lung volume more quickly than the reduction in lungs inflated with room air, and this may have decreased the injury caused by hyperinflation during storage.
In the lungs hypoinflated with room air, Kf increased significantly in comparison with that in normally inflated lungs. In the 50% O2 and 100% O2 groups, however, this deterioration was not observed. On the basis of the results of our lung volume study, it is likely that the volume of lungs inflated with 50% O2 decreased more than the volume of those inflated with room air. This suggests that decreased lung volume was not the only cause of deterioration in Kf of lungs hypoinflated with room air. Date and associates 19 demonstrated that intraalveolar O2 concentration after 24 hours of preservation (10° C) was less than 6% when rabbit lungs were inflated with room air at 10 ml/kg. It is possible that in lungs hypoinflated with room air available O2 may be insufficient to maintain aerobic metabolism during prolonged storage. Furthermore, lung volume and airway pressure of lungs hypoinflated with room air changed minimally after 12-hour preservation (Tables I and II). This supports our speculation that a lack of O2 may be a main cause of deterioration in Kf and that deterioration tends to occur after 12 hours of preservation when lungs are stored at low volumes and low O2 concentrations.
In the 100% O2 inflation group, at any inflation volume, Kf was significantly increased. Although the exact mechanism of this deterioration is unclear, we believe that O2 free radical injury during storage is at least partly responsible. With use of the same model we have demonstrated that the free radical scavenger dimethylthiourea improved pulmonary capillary permeability of lungs subjected to prolonged storage while inflated with 100% O2. 20
It has been previously reported that permeability edema occurred when lungs were ventilated at a high tidal volume, irrespective of airway pressure. 12,21,22 Irrespective of the type of pulmonary distention produced, the same proportion of protein leakage and water filtration into the extravascular space occurred. 21 The extent of the stress failure in the capillary wall has been assessed by morphometric analysis. 23,24 Those reports demonstrated that there was a large increase in the frequency of stress failure of the capillary endothelium at higher lung volumes. Those findings may provide a physiologic mechanism for increased pulmonary capillary permeability at high states of lung inflation in our current study.
Puskas and associates 5 recently reported that hyperinflated canine lung allografts had excellent gas exchange function immediately after implantation. The assessment of lung function done in their study was conducted after 10 minutes of contralateral, native pulmonary artery occlusion, with both lungs ventilated. We have shown here that airway resistance was lower in the hyperinflated lung after 24-hour storage. Hence, in the study of Puskas and associates 5 it is possible that higher airway resistance in this control group (normal lung volume) increased the ventilation-perfusion mismatch thereby decreasing arterial O2 tension. Furthermore, it is possible that a brief 10-minute period of assessment with contralateral pulmonary artery occlusion is inadequate to evaluate the predisposition of an allograft to edema formation.
On the basis of findings in our previous canine study, 5 we adopted a policy of hyperinflation during flush and storage in our clinical lung transplant program. Unfortunately, this was followed by an increased prevalence of immediate postoperative allograft edema. As a result of this experience, the results reported here, and the results from a companion study in canine lung allografts, 25 we have returned to a policy of normal volume inflation during flush and end-tidal volume inflation during storage.
In summary, this study demonstrated that intraalveolar O2 concentration affects lung volume and airway pressure during 24-hour preservation. Inflation with 100% O2 during storage increases pulmonary vascular permeability. Furthermore, static hyperinflation during storage increases pulmonary capillary permeability, irrespective of storage inspired O2 fraction.
Acknowledgments
We acknowledge the secretarial support of Mrs. Dawn Schuessler and Mary Ann Kelly.
References
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