Vascular distension and continued ventilation are protective in lung ischemia/reperfusion.

Biophysical factors have been implicated in the development of pulmonary ischemia-reperfusion injury. In isolated rabbit lungs, the impact of vascular and alveolar distension, with and without alveolar oxygen supply, was investigated. With interruption of both perfusion (zero intravascular pressure) and ventilation, reperfusion after 120 min of warm ischemia resulted in transient pulmonary hypertension, with largely unchanged microvascular pressures, followed by a dramatic leakage response with approximately 10-fold increased capillary filtration coefficients (Kfc) and severe edema. Maintenance of vascular distension during ischemia (intravascular pressure of approximately 2 to 3 mm Hg) reduced the hypertension and fully suppressed the leakage. Employing ischemic periods of 180 and 240 min, ventilation of the lungs with 21 or 100% oxygen > ventilation with nitrogen during perfusion stop, but not static anoxic inflation, further enhanced the protective effect of vascular distension. At optimal biophysical support (vascular distension and ongoing normoxic ventilation), even 240 min of warm ischemia was tolerated with only moderate Kfc increase. We conclude that biophysical factors exert marked influence on pulmonary ischemia-reperfusion injury. Maintenance of vascular distension possesses strong protective potency, further enhanced by continued ventilation and alveolar oxygen supply during ischemia. These results may have important implications for organ preservation in lung transplantation.