Effects of cigarette smoking on the function of metabolizing arachidonic acid and angiotensin I in the isolated perfused rat lungs

Summary

The effects of acute and chronic cigarette smoking on the metabolism of exogenous arachidonic acid (AA) and angiotensin I (AI) in perfused isolated rat lungs were studied. The results showed that acute cigarette smoking did not alter the contents of 6-keto-PGF_1α (the stable metabolite of PGI₂) and TXB₂ (the stable metabolite of TXA₂) in the effluent and the increment of pulmonary artery pressure (†P_pa) caused by AA. The conversion of A I into A II was significantly increased (P<0.01), while the †P_{p a}, induced by A I injection was obviously decreased as compared with controls (P<0.05). After cigarette smoke exposure for 30 days, the †P_{p a} caused by AA or A I did, not differ from that of controls, but the contents of 6-ketoPGF_1α and A II increased more markedly than those in non-smoking rats,(P< 0.05). It is suggested that acute and chronic cigarette smoking in rats can promote the lung function of converting A I into A II, chronic smoking can increase the lung function of metabolizing AA into PGI₂.