Journal
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS
Volume 68, Issue 3, Pages 191-195Publisher
ELSEVIER SCI LTD
DOI: 10.1016/S0952-3278(02)00229-6
Keywords
isolated heart; myocardial ischemia; nicotine; prostacyclin; thromboxane
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It has been proven that nicotine contributes to cardiovascular diseases, although its precise mechanism of action is still unclear. The purpose of this study is to find how nicotine may complicate myocardial ischemia by affecting the thromboxane/prostacyclin (TXA(2)/PGI(2)) balance. We used four groups (n = 7 each) of isolated and perfused rabbit hearts according to Langendorff method: (i) control group; (ii) group submitted to 1 muM nicotine perfusion during 60 min; (iii) group submitted to a regional ischemia by ligation of the left descending coronary artery during 60 min and (iv) group submitted to nicotine perfusion during ischemia. Levels of TXB(2) and 6-keto PGF(1alpha), the stable metabolites of TXA(2) and PGI(2) were then determined in the microsomes of the hearts by radioimmunoassay. The results showed that (1) a TXA(2) synthetase activity is present in the myocardium, and this activity, as well as that of PGI(2) synthetase, is decreased by a 60 min ischemia; (2) TXA(2) and PGI(2) activities are not affected by nicotine in the normal myocardium and (3) nicotine infusion during ischemia contributes to the increase of TXA(2)/PGI(2) ratio further by decreasing PGI(2). Therefore, these results provide one explanation on how nicotine might worsen myocardial ischemia. (C) 2003 Elsevier Science Ltd. All rights reserved.
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