[Influence of cigarette smoking on the hypoxic pulmonary vasoconstriction in isolated rat lungs--the role of prostaglandins and leukotrienes]

Abstract

Isolated rat lungs perfused with blood were used to determine the effects of cigarette smoke, delivered into the lung by a ventilator, on the pulmonary vascular resistance (PVR), and on the hypoxic pulmonary vasoconstriction (HPV), and to explore the role the prostaglandins (PG) and leukotrienes (LT) play in that effect. The results showed that PVR did not change, while HPV was significantly enhanced by smoking. Indomethacin, an inhibitor of PG biosynthesis, administered in the perfusing blood (20 micrograms/ml) increased HPV in non-smoking lungs, but not in lungs after smoking. Diethylcarbamazine citrate (DEC; 1 mg/ml), an inhibitor of LT biosynthesis, decreased HPV before and after smoking. After perfusion with both indomethacin and DEC, HPV also decreased. It is suggested that LT act as mediators whereas PG as modulators in HPV, and PG and LT might play an important role in the increase of HPV by cigarette smoking.