PLATELET-ACTIVATING-FACTOR INDUCES SELECTIVE PULMONARY ARTERIAL HYPERREACTIVITY IN ISOLATED-PERFUSED RABBIT LUNGS

The role of vasoreactivity in PAF-induced pulmonary hypertension (PHT) was assessed in isolated, perfused rabbit lungs. We evaluated the ste ady-state pulmonary vascular response to five vasoconstrictors: PGF2al pha, norepinephrine, angiotensin II, PAF, and KCl. Pulmonary arterial pressure and pulmonary vascular resistance (PVR) were significantly gr eater in lungs of rabbits treated with PAF for 28 days than in control rabbits in response to PGF2alpha and norepinephrine. When resistance was partitioned by the vascular occlusion method, at baseline the vasc ular resistance was equally distributed between arterial and venous se gments in both experimental groups. Arterial resistance accounted for approximately 76% of PVR during norepinephrine injection and 60% of PV R during PGF2. injection in PAF-treated lungs. Whereas arterial resist ance accounted for approximately 63% of PVR during norepinephrine inje ction and 52% of PVR during PGF2alpha injection in control lungs, ther e was no significant difference in the response to angiotensin II, acu te PAF, and KCl in lungs from chronic PAF-treated rabbits compared wit h responses in control rabbit lungs, though the pressor response to ac ute PAF tended to be blunted in PAF-treated lungs. Chronic PAF treatme nt results in enhanced pulmonary arterial reactivity to selected autac oids in isolated perfused lungs.