Hemodynamic effects of brief pulmonary hemostasis

We determined the hemodynamic effects of brief hemostasis in isolated blood-perfused rat lungs held at constant inflation pressure. Three periods of hemostasis, each lasting 20 min, alternated with equal durations of perfusion. Pulmonary vascular resistance (PVR), calculated as the ratio of the pulmonary arterial- (Ppa) left atrial (Pla) pressure difference to flow, was determined at baseline and after the third hemostasis period. Hemostasis increased PVR by 127% above baseline at constant Ppa and Pla (n = 8; P < 0.05) and by 71% at constant Pla and constant flow (n = 16; P < 0.05). The PVR increases were significantly attenuated by platelet (n = 5) or red blood cell (n = 4) removal from the lung perfusion, mechanical ventilation (n = 5), indomethacin (2 X 10(-6) M; n = 5), papaverine (10(-5) M; n = 4), and the thromboxane blocker SQ-29548 (7.8 X 10(-5) M; n = 4). By micropuncture we determined that the posthemostasis increase of the total pressure drop was 66% due to an increase of the venous pressure drop (P < 0.05). Isogravimetric pressure and lung water were not significantly altered by hemostasis. We conclude that brief hemostasis in the rat lung induces platelet- and red blood cell-dependent increase of vascular resistance. This effect may be attributable to hemostasis-induced platelet activation leading to thromboxane release.