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J Thorac Cardiovasc Surg 1994;107:1193-1202
© 1994 Mosby, Inc.
CARDIOPULMONARY BYPASS, |
Saskatoon, Saskatchewan, Canada
Supported by a grant from the Canadian Heart and Stroke Foundation.
Received for publication May 19, 1993. Accepted for publication Nov. 8, 1993. Address for reprints: David Johnson, MD, Box 95, Royal University Hospital, Saskatoon, Saskatchewan, Canada S7N 4J9.
Abstract
A pulmonary injury of varying severity occurs routinely after cardiopulmonary bypass. We studied the pulmonary complications of partial cardiopulmonary bypass in four groups of dogs to better define the injury and to evaluate the efficacy of two interventions (addition of a leukocyte filter or cyclooxygenase inhibition) on preservation of systemic oxygenation. All animals received a standard anesthetic (pentobarbital, morphine, and vecuronium) and, after sternotomy, three groups of animals received 3 hours of partial cardiopulmonary bypass. The animals were randomized to receive partial bypass alone (n = 6), indomethacin and bypass (n = 5), or a leukocyte filter and bypass (n = 5). A fourth group (n = 5) did not receive bypass and served as a time control. We measured blood gases and also obtained histologic samples to assess the degree of lung injury. We found that bypass alone caused a significant reduction (p < 0.05) in arterial oxygen tension 1 hour after the conclusion of bypass (175 ± 53 mm Hg) compared with prebypass values (357 ± 41 mm Hg). Pretreatment with indomethacin ameliorated the decrease in arterial oxygen tension from prebypass to postbypass values (477 ± 50 mm Hg versus 339 ± 57 mm Hg, respectively). Similarly use of a leukocyte filter reduced the decline in arterial oxygen tension from prebypass to postbypass values (440 ± 71 mm Hg versus 311 ± 73 mm Hg, respectively). We believe that indomethacin ameliorates the decline in systemic oxygenation associated with bypass by augmentation of hypoxic pulmonary vasoconstriction and that the leukocyte filter acted to reduce pulmonary edema and thereby minimized intrapulmonary shunt. (J THORACCARDIOVASCSURG1994;107:1193-1202)
After cardiopulmonary bypass (CPB), patients may exhibit the pump lung syndrome, an injury indistinguishable from the adult respiratory distress syndrome. 
1-5 Neutrophil activation, central to the development of adult respiratory distress syndrome, 6 may also cause the pump lung syndrome. In both conditions there is increased microvascular margination of neutrophils, 6,7 as well as altered neutrophil function. 8-10 Although the pump lung syndrome is uncommon, histologic criteria for adult respiratory distress syndrome is found in 12% of patients who die after coronary artery bypass. 11
This study examines the effects of extracorporeal bubble oxygenation on indices of gas exchange, pulmonary edema, and the expression of hypoxic pulmonary vasoconstriction. 12 We evaluated whether a leukocyte filter 13 inserted into the bypass circuit or pretreatment with indomethacin could modify the pulmonary injury. In this manner we hoped to better understand the factors that cause lung injury after CPB and to evaluate two interventions that might minimize the injury.
METHODS
Animal preparation
These studies, done with the approval of our University Animal Care Committee, are in compliance 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" published by The National Institutes of Health. Twenty-one mongrel dogs (20 to 28 kg) were anesthetized with pentobarbital (15 mg/kg), tracheally intubated, and the lungs ventilated (respiratory pump, model No. 607, Harvard Apparatus, Dover, Mass.) at a tidal volume of 15 ml/kg with 100% O2. Throughout the remainder of the experiment, the respiratory rate was adjusted to maintain arterial carbon dioxide tension (PaCO2) between 25 and 40 mm Hg and arterial pH between 7.30 and 7.45. The animals were heparinized (5000 units by intravenous bolus followed by 1000 units/hr intravenously) and anesthesia was maintained by a constant infusion of pentobarbital (1.0 mg/kg per hour), morphine (0.1 mg/kg per hour), and vecuronium (0.1 mg/kg per hour). A pulmonary artery catheter was used to measure mean pulmonary artery pressure, pulmonary capillary wedge pressure, and cardiac output (CO) by thermodilution (Edwards-Baxter model No. 9520A, Santa Ana, Calif.). Transducers were leveled to midchest and all values were recorded (Space Labs model No. 510, Squibb, Hollsboro, Ore.).
Bilateral femoral arteriovenous fistulas were created by placing tapered catheters (8F) connecting the right femoral vein to the right femoral artery and connecting the left femoral vein to the left femoral artery. With the use of a three-way connector and clamps, each arteriovenous femoral fistula could be individually open to flow or occluded. The femoral fistulas were subsequently used to alter CO (see following section) and obtain a pressure-flow (P-Q) relationship for the pulmonary vasculature. The catheters were also used as part of the bypass circuit during extracorporeal oxygenation. The pericardium, exposed by a midline sternotomy, was incised and a catheter was inserted through the left atrial appendage to measure left atrial pressures. A cuffed double-lumen endotracheal tube (36F) was positioned via a tracheostomy to allow independent right and left lung ventilation.
Experimental protocol
The measurements during 100% O2 ventilation at time 0 constituted period O2t = 0. We measured levels of 6-keto-prostaglandin F1
(6-keto-PGF1), malondialdehyde, and thromboxane B2; neutrophil chemoluminescence; white cell count with differential; arterial and mixed venous blood gases; and oxyhemoglobin saturations. Hemodynamic measurements included CO, mean arterial pressure, pulmonary artery pressure, and pulmonary capillary wedge pressure. In addition, the P-Q relationship was obtained by altering CO through manipulation of the femoral fistulas and measuring the resultant pressures and flows. Initially both of the arteriovenous fistulas were closed and then to alter flow first one arteriovenous fistula was opened, then the second fistula was opened, and finally both fistulas were closed.
We next ventilated the left lung with 100% N2 and the right lung with 100% O2 with the use of two separate ventilators connected to the individual lumina of the double-lumen tracheal tube. The left lung was ventilated at 40% of the original tidal volume while the right lung was ventilated at 60% of the original tidal volume, thereby approximating the normal tidal volume of each lung. After 15 minutes all hemodynamic, gas exchange, and P-Q measurements were obtained as outlined herein and this constituted period O2/N2t = 0.
Fifteen dogs were randomized to receive partial CPB and six dogs served as a control group. In the dogs randomized to receive partial CPB, a cannula was inserted into the right atrium. Blood from the atrium was pumped at a flow rate of 100 ml/kg (2M6002 Travenol, Morton Grove, Ill.) through a bubble oxygenator (Polystan, Copenhagen, Denmark) and returned to the aorta. The oxygenator received gas flow consisting of 95% O2 and 5% CO2. The animals were cooled to 24° C over 30 minutes and the extracorporeal circulation was maintained for a further 2 hours. The circuit was primed with 2 L of electrolyte solution (Normosol-R D5-W) and a further 3 to 4 L was subsequently infused to maintain an adequate volume. Any blood that collected within the mediastinum was reinfused to maintain right atrial pressure between 7 and 10 mm Hg and mean arterial pressure greater than 100 mm Hg. After 2 hours the animals that received partial CPB were warmed to 37° C over 30 minutes and then CPB was discontinued. In this manner total bypass time was 3 hours. During rewarming, mechanical ventilation was recommenced with 100% O2 and sodium bicarbonate was infused as needed.
Four hours after the start of CPB all measurements, including the P-Q relationship, were repeated during 100% O2 ventilation (period O2t = 4). Again, similar to period O2/N2t = 0, measurements were repeated during ventilation of the left lung with 100% N2 and right lung with 100% O2 (period O2/ N2t = 4). The animals were then killed and the lungs exsanguinated and removed for subsequent histologic examination.
Experimental interventions
The animals were randomized into four groups: the CPB group (n = 5) received partial CPB alone; the indomethacin-CPB group (n = 5) received partial CPB but also received 12.5 mg/kg indomethacin during instrumentation and again at the end of bypass; the filter-CPB group (n = 5) received partial CPB with a leukocyte filter (Pall LG-6, Pall Biomedical Products Corp., Glen Cove, N.Y.) inserted between the roller pump and arterial filter; the control group (n = 6) did not receive CPB (Fig. 1). The animals in the control group received mechanical ventilation of the lungs throughout the experiment and were maintained euthermic. All four groups had measurements and assays obtained at similar times and received similar volumes of fluid (3 to 4 L). Although the control group did not undergo bypass, for consistency measurements obtained during baseline conditions are described as prebypass and measurements obtained at 4 hours are described as postbypass measurements.
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Mixed venous and arterial blood gases were measured at 37° C and temperature corrected. 14 Oxyhemoglobin saturations were measured by co-oximetry (model OSM2, Radiometer A/S, Copenhagen, Denmark). Intrapulmonary shunt was calculated from the standard shunt equation but, because of technical considerations, could not be measured during periods of N2 ventilation. 6-Keto-PGF1and thromboxane B2were measured by high-performance liquid chromatography and radioimmunoassay. 15Plasma tumor necrosis factorlevels were measured by immunoenzymatic assay (TNF-EASIA, Medgenix Diagnostics, Brussels, Belgium) and plasma malondialdehyde levels were fluorometrically measured. 16Neutrophil chemiluminescence was measured in terms of the neutrophil capacity to inhibit the photoreduction of nitroblue tetrazolium by riboflavin and methionine. 17
Edema and lung histologic study
The lungs were inflated to 35 cm H2O and a sample from the right lower lobe was fixed. Five-micrometer sections were cut and stained with hematoxylin and eosin. Qualitative assessment of the presence of granulocytes and edema was made in 10 microscopic fields (0.05 mm2). Granulocytes or fluid found in either the alveolar or peribronchial spaces were graded as present (1) or absent (0) and an individual point score recorded. The wet weight of the excised lungs was measured and the lungs air-dried until a constant weight was recorded (dry weight). The wet/dry weight was used as a separate index of pulmonary edema.
Statistics
Values of arterial O2 tension (PaO2), thromboxane B2, 6-keto-PGF1, and malondialdehyde between groups were compared by a two-way analysis of variance and within-period comparisons were made by one-way analysis of variance. Where appropriate, paired ttests with correction for the number of comparisons 18were used to determine which periods or groups were different. We prospectively limited comparisons to period O2t = 0versus period O2t = 4, period O2/N2t = 0versus period O2/N2t = 4, period O2t = 0versus period O2/N2t = 0, and period O2t = 4versus period O2/N2t = 4. Between-group comparisons were limited to the control group versus the other three groups. A pvalue < 0.05 was considered as significant. The slopes and intercepts of the P-Q relationships were compared as described by Feldman. 19Lung edema scores were compared by cross-table tabulation and
2. All values are given as mean ± standard deviation.
RESULTS
Hemodynamics and blood gases
Tables I, A through D, illustrates group mean values for selected blood gases and hemodynamics. Values of CO and pulmonary capillary wedge pressure were similar between groups and over time. During ventilation with 100% O2, values of PaO2 decreased after bypass except in the control group (Fig. 2). Postbypass values of PaO2 and intrapulmonary shunt were significantly worse than control group values only in the CPB group. As expected, PaO2 was lower during N2 ventilation as compared with that value during periods of 100% O2 ventilation; however, only in the CPB group were values of PaO2 during N2 ventilation significantly decreased from prebypass to postbypass. Also, during the same period, values of arterial O2 saturation in the CPB group showed clinically significant decreases to 77% ± 16% but remained higher than 90% in the other groups.
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(Table II). Values of Pcrit increased during both periods of N2 ventilation compared with those during 100% O2 ventilation in the indomethacin-CPB group. After bypass Pcrit also increased in the CPB group during N2 ventilation compared with the values during 100% O2 ventilation. Pcrit increased from period O2t = 4 to period O2/N2t = 4 in all groups but the filter-CPB group.
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(Table III) but the indomethacin-CPB and the filter-CPB groups had lower edema scores than did the control and the CPB groups. Granulocyte infiltration was not detected by routine histologic study in any lobes independent of pulmonary hemorrhage. The indomethacin-CPB group had lower levels of 6-keto-PGF1compared with those of the control group both before and after bypass. Within each group values for 6-keto-PGF11and thromboxane B2did not change significantly from prebypass to postbypass (Fig. 4). Values of malondialdehyde were similar between groups over time but because of technical difficulties were not available in the indomethacin-CPB group (Fig. 5). After bypass, values of chemiluminescence decreased in the filter-CPB group from prebypass to postbypass (Fig. 5) and postbypass values were significantly lower than control group values. Otherwise chemiluminescence was similar between groups and over time.
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Experimental model
These studies were designed to investigate the specific effects of extracorporeal circulation on gas exchange and hypoxic pulmonary vasoconstriction. Therefore we avoided the confounding features associated with cessation of pulmonary flow and the subsequent reperfusion. Although reperfusion may be important in causing injury, 20 extracorporeal circulation alone may be sufficient. 21 We elected to accentuate the degree of pulmonary injury associated with bypass by using a bubble oxygenator rather than a membrane oxygenator 22 and by using a prolonged period of extracorporeal circulation (3 hours). We prospectively controlled parameters that might independently influence systemic oxygenation or edema formation. In adult respiratory distress syndrome, edema formation and intrapulmonary shunt are influenced by the microvascular hydrostatic pressure 23 and CO, 24 respectively. We therefore maintained levels of left atrial pressure and CO comparable between groups and over time. Also, our anesthetic agents, pentobarbital and morphine, do not affect measurements of PVR. 25 Therefore we are confident that any differences in edema, gas exchange, or hypoxic pulmonary vasoconstriction over time or between groups were a result of the experimental interventions.
PVR
Although we measured PVR as a pressure (pulmonary artery pressure – pulmonary capillary wedge pressure) required to generate flow (CO) through the pulmonary vasculature, the use of P-Q plots allows a more precise description of resistance. 26 The incremental resistance is the inverse of the slope of the P-Q relationship whereas the Pcrit is the extrapolated zero-flow pressure intercept. Pcrit may reflect vascular tone and the incremental resistance may reflect vascular cross-sectional area. 26 Hypoxia increases Pcrit with minimal effects onincremental resistance. 27
During 100% O2 ventilation, PVR tended to increased over the 4-hour experimental period. The increase in PVR was statistically significant only in the time control group, which suggests that it was a nonspecific feature of the experimental procedure alone. Examining the P-Q relationship, we found the incremental resistance to be similar between all periods and between groups. Pcrit, on the other hand, tended to increase over the course of the study with the increase statistically significant only in the indomethacin-treated group. However, the lack of other statistical significance comparisons may reflect our extremely conservative test.
PVR uniformly increased during N2 ventilation compared with 100% O2 ventilation, suggesting that hypoxic pulmonary vasoconstriction was present in all four groups even after bypass. Values of incremental resistance were unchanged over time in all groups but Pcrit increased significantly during N2 ventilation in the indomethacin-treated group both before and after bypass. We found that indomethacin treatment reduced levels of 6-keto-PGF1, an index of prostaglandin I2production, confirming the augmentation of hypoxic pulmonary vasoconstriction by inhibition of concurrent release of a prostaglandin I2 28,29After bypass, Pcrit also increased significantly in the CPB group during N2ventilation, likely because of the effects of the extremely low mixed venous PO2 30Pcrit did not increase during N2ventilation in the group treated with a leukocyte filter. It is possible that removal of activated leukocytes altered vascular reactivity by preventing the release of a nonprostaglandin vasoconstrictor. 31Thus we believe that bypass causes activation of leukocytes with release of pulmonary vasoconstrictors, which then increases PVR. 32,33
Pump lung
We could not detect leukocytes by routine histologic examination, but our interventions did affect levels of circulating neutrophils with levels increasing by 4 hours, but only in the control group. It is possible that with partial bypass the stimulus for leukocyte sequestration is not as great as in the human setting of complete bypass. However, similar to prior studies, 34 we found impaired gas exchange and worsened intrapulmonary shunt in the CPB group after bypass. Use of indomethacin or a leukocyte filter attenuated the bypass-induced decrease in PaO2, with intrapulmonary shunt unchanged in the indomethacin-treated group and improved in the group treated with a leukocyte filter. Not unexpectedly, during ventilation of the left lung with 100% N2, PO2 decreased further in all groups. However, in the animals treated with indomethacin or with the leukocyte filter, this decrease was also attenuated. Compared with results in the bypass group there was less edema by histologic study in the groups treated with indomethacin or leukocyte filter, which suggests that the improvement in PO2 may have been caused by a reduction in alveolar edema. Alternatively, indomethacin has been previously shown to augment HPV, 35 and that might account for the relative preservation of gas exchange in the indomethacin-treated animals.
Depletion of leukocytes has been previously shown to improve systemic oxygenation after bypass. 33,34 Although the leukocyte filter did not reduce the total number of leukocytes, it did reduce leukocyte activation, as assessed by chemiluminescence. Neutrophils release several products, including proteolytic enzymes and oxygen free radicals, 22 which can result in an acute lung injury. Cytokine release may further aggravate the tissue injury, but we did not find increased levels of tumor necrosis factor even though our assay was sensitive for canine tumor necrosis factor . 36 This suggests that tumor necrosis factor is not necessary to produce the acute lung injury. Oxygen free radicals can cause cell membrane lipid peroxidation, 32 and this results in elevation of serum malondialdehyde. 37 Although bypass may increase lipid peroxidation, 32,34 our study also suggests that it is not necessary to cause the altered pulmonary vasoactivity. Finally, we found that indomethacin improved gas exchange after bypass by reducing prostaglandin I2 production, but prostaglandin I2 has been shown to reduce free radical generation. 37 Thus the acute effects of treatment with indomethacin may result in improved gas exchange but at a theoretic cost of longer-term increases in the pulmonary injury.
In summary, we found that partial bypass alone was associated with a mild pulmonary vascular injury. This injury resulted in impaired gas exchange and systemic hypoxia. The systemic hypoxia could be prevented by pretreatment with indomethacin or by use of a leukocyte filter. These two interventions acted through different mechanisms; indomethacin augmented hypoxic pulmonary vasoconstriction and thereby improved gas exchange whereas the leukocyte filter reduced pulmonary edema and thereby improved gas exchange. Our studies suggest that modulation of leukocyte function offers a means of reducing the pulmonary injury commonly associated with CPB. The use of a leukocyte filter may alter leukocyte function without the hazards associated with drugs such as indomethacin.
Acknowledgments
We acknowledge the expert technical and secretarial assistance of Terry Cannon and Anita Zacharias.
Footnotes
From the Departments of Anesthesia,a Medicine,b Surgery,c Physiology,d Pharmacology,e and Pathology,f University of Saskatchewan, Saskatoon, Saskatchewan, Canada. 
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