VASCULAR EFFECTS OF CIGARETTE-SMOKE IN ISOLATED PIG LUNGS

Abstract

To determine the local effects of cigarette smoke on the pulmonary vasculature, pulmonary artery pressure-flow curves in isolated, blood-perfused pig lungs before and after 4 exposures to cigarette smoke were measured. During each exposure, smoke was administered into the trachea for 3-4 min at a rate of 20-25 puffs/min and a puff volume of 35-50 ml with a smoking machine. During hypoxia (inspired PO2 [O2 partial pressure], 50 mm Hg), when baseline vasomotor tone was high, cigarette smoke caused an acute transient vasodilation. During control (inspired PO2, 200 mm Hg), when baseline tone was low, no significant effect was observed. In addition to this acute effect, cigarette smoke depressed the pulmonary pressor response to hypoxia, which developed gradually during the course of the experiment. Indomethacin, at perfusate concentrations of 20 and 100 .mu.g/ml, did not significantly alter the acute vasodilating effect of smoking, suggesting that prostaglandins synthesized by cyclooxygenase were not the mediators of this response. Indomethacin did prevent the gradual depression of the pulmonary vasoconstrictor response to hypoxia.