The metabolism of arachidonic acid in isolated rat lungs is not changed during cigarette smoke ventilation

Abstract

Cigarette smoke ventilation of isolated perfused rat lungs partially inhibited the pulmonary vascular pressor response to arachidonic acid. The amounts of metabolites of exogenous arachidonic acid in the perfusion effluent remained unchanged during smoke ventilation. The antiaggregatory effect of the effluent during pulmonary infusion of AA was not decreased by smoke ventilation. The cause of the previously reported increased platelet aggregation after smoking remains unclear.