The effect of cigarette smoke on the metabolism of arachidonic acid to myotropic compounds in rat and hamster isolated lungs

Abstract

Perfusion effluent from isolated rat and hamster lungs caused a relaxation of superfused strip of bovine coronary artery (BCA). This relaxation was abolished by pulmonary infusion of indomethacin. Pre-exposure of rats and hamsters to cigarette smoke during half an hour before the lung perfusion did not change the degree of this initial relaxation of BCA. Injection of 10 μg of sodium arachidonate (AA) into the pulmonary circulation of isolated hamster lungs caused a contraction of BCA, which was not changed by cigarette smoke pre-exposure. When AA (10 μg) was injected into the pulmonary circulation of isolated hamster lungs during cigarette smoke ventilation the contractions of superfused BCA and rat stomach strip (RSS) were not significantly different from those during the preceding and following air ventilation. In experiments with isolated rat lungs the initial relaxation of superfused BCA was accompanied by a contraction of superfused RSS. AA injection (10 μg) into rat lungs caused a further relaxation of BCA and contraction of RSS, which were abolished by pulmonary infusion of indomethacin. Cigarette smoke ventilation of isolated rat lungs caused a relaxation of superfused BCA, which was not abolished by indomethacin. During cigarette smoke ventilation injection of AA (10 μg) into the pulmonary circulation of rat lungs caused a relaxation of BCA and a contraction of RSS.

The present study indicates that neither cigarette smoke ventilation nor pre-exposure to cigarette smoke has a drastic effect on the metabolism of arachidonic acid to myotropic compounds in isolated hamster and rat lungs.