PAF INCREASES CAPILLARY-PRESSURE BUT NOT VASCULAR-PERMEABILITY IN ISOLATED BLOOD-PERFUSED CANINE LUNGS

We determined the effects of platelet-activating factor (PAF) on pulmo nary vascular resistance, lung weight, and microvascular permeability in isolated canine lungs perfused at constant pressure with autologous blood. PAF caused a dose-dependent increase in total pulmonary vascul ar resistance (R(t)) and pulmonary capillary pressure assessed as doub le-occlusion pressure. PAF (33 mug; n = 7) caused a 10-fold increase i n R(t) and a decrease in precapillary-to-postcapillary vascular resist ance ratio from 0.97 +/- 0.10 to 0.38 +/- 0.03, suggesting predominant pulmonary venoconstriction. Shortly after PAF, lung weight decreased transiently and then increased, reaching a plateau above baseline (112 .5 +/- 1.6%) at 30 min. In lungs perfused in the antidromic direction from the pulmonary vein to the artery (n = 5), PAF (33 mug) produced m arked precapillary vasoconstriction, consistent with pulmonary venocon striction, and a remarkable and sustained decrease in lung weight belo w baseline by 30 min. Vascular permeability, measured 30 min after PAF using the capillary filtration coefficient and isogravimetric capilla ry pressure, did not change significantly from baseline. Thus we concl ude that PAF produces lung weight gain by means of an increase in capi llary pressure predominantly due to pulmonary venoconstriction without significant changes in vascular permeability in isolated blood-perfus ed canine lungs.