Cardiovascular surgery requiring cardiopulmonary bypass (CPB) is frequently complicated by postoperative lung injury. Bronchial artery (BA) blood flow has been hypothesized to attenuate this injury. The purpose of the present study was to determine the effect of BA blood flow on CPB-induced lung injury in anesthetized pigs. In eight pigs (BA ligated) the BA was ligated, whereas in six pigs (BA patent) the BA was identified but left intact. Warm (37°C) CPB was then performed in all pigs with complete occlusion of the pulmonary artery and deflated lungs to maximize lung injury. BA ligation significantly exacerbated nearly all aspects of pulmonary function beginning at 5 min post-CPB. At 25 min, BA-ligated pigs had a lower arterial Po2at a fraction of inspired oxygen of 1.0 (52 ± 5 vs. 312 ± 58 mmHg) and greater peak tracheal pressure (39 ± 6 vs. 15 ± 4 mmHg), pulmonary vascular resistance (11 ± 1 vs. 6 ± 1 mmHg·l–1·min), plasma TNF-α (1.2 ± 0.60 vs. 0.59 ± 0.092 ng/ml), extravascular lung water (11.7 ± 1.2 vs. 7.7 ± 0.5 ml/g blood-free dry weight), and pulmonary vascular protein permeability, as assessed by a decreased reflection coefficient for albumin (σalb; 0.53 ± 0.1 vs. 0.82 ± 0.05). There was a negative correlation ( R = 0.95, P < 0.001) between σalband the 25-min plasma TNF-α concentration. These results suggest that a severe decrease in BA blood flow during and after warm CPB causes increased pulmonary vascular permeability, edema formation, cytokine production, and severe arterial hypoxemia secondary to intrapulmonary shunt.
Cardiopulmonary bypass reduction of bronchial blood flow: A potential mechanism for lung injury in a neonatal pig model