急、慢性吸烟对大鼠肺代谢花生四烯酸血管紧张素及其血管反应性的影响  

Effects of Cigarette Smoke on Fate of Archdonic Acid and Angiotensin I and Vascular Activity in Purfused Isolated Lungs

作　　者：于小玲[1] 金咸瑢 王迪浔[1] 

机构地区：[1]山东滨州医学院,同济医科大学病理生理教研室

出　　处：《中国公共卫生学报》1996年第4期215-217,共3页

摘　　要：大鼠急性吸烟５ｍｉｎ及慢性吸烟３０天后，观察离体肺代谢外源性花生四烯酸（ＡＡ）、转化血管紧张素Ⅰ（ＡⅠ）及其血管反应性的变化．结果发现大鼠离体灌流肺吸烟５ｍｉｎ时注入ＡＡ，流出液中前列环素（ＰＧＩ２）的代谢物６－酮－ＰＧＦ１ａ和血栓素Ａ２（ＴＸＡ２）的代谢物ＴＸＢ２及肺动脉灌注压增值（★　ｐａ）与对照组无明显差异；注入ＡⅠ后，★Ｐｐａ低于对照组，而ＡⅠ转化为ＡⅡ的量明显高于对照组（Ｐ＜０．０１）．吸烟３０天后的大鼠离体肺，同样注入ＡＡ或ＡⅠ时，★Ｐｐａ均无明显改变，而流出液中６－铜－ＰＧＦ１ａ和ＡⅡ的量均显著高于对照组（Ｐ＜０．０５），说明吸烟可以改变肺的代谢功能，急性吸烟可降低肺对血管紧张素的反应性．The effects of acute and chronic cigarette smoking on the metabolism of exogenous archidonic acid(AA)and angiotensin I(AI)and the ascular activity in perfused isolated rat lungs werestudied. The results showed that acute cigarette smoking did not alter the contents of 6-keto-PGFla(the stable metabolite of PGI2)and TXB2(the stable metabolite of TXA2)in the effluent and the increment of pulmonary artery pressure(★Ppa) caused by AA.The conversion of AI into A I was significantly increased(P<0.01),while the ★Ppa induced by AI injection was obviously decreased as compared with controls(p<0.05).After cigarette smoke exposure for 30days.the ★Ppa caused by AA or AI did not differ from that of cuntrols, but the contents of 6-keto-PGFla and AII increased more markedly than that in non-smoking rats(P<0.05).It is suggested that cigarette smoking can affect part lung function of melabolism and vascular activity,acute cigarette smoking can depense the activity of pulmonary vasoconstriction to angiotensin.

关 键 词：吸烟 肺代谢 花生四烯酸 血管紧张素 

分 类 号：R163[医药卫生—公共卫生与预防医学]