Hoshida S, Kuzuya T, Nishida M, Kim Y, Kitabatake A, Kamada T, Tada M
First Department of Medicine, Osaka University School of Medicine, Japan.
Am J Cardiol. 1989 Mar 7;63(10):24E-28E. doi: 10.1016/0002-9149(89)90226-9.
To assess the role of neutrophils and arachidonate metabolites in evolving myocardial infarction, the effect of inhibitors of arachidonate metabolism on the extent of myocardial damage and neutrophil function was examined in a 90-minute occlusion/5-hour reperfusion model of canine myocardial infarction. A thromboxane A2 synthetase inhibitor, CV-4151, and a lipoxygenase inhibitor, AA-861, greatly reduced the infarct size. They also attenuated the production of chemoattractant leukotriene B4 and chemotactic activity of neutrophils isolated from peripheral circulation. Under these conditions, both the increases in peripheral leukocyte count and neutrophil infiltration in ischemic myocardium were inhibited. These results indicate that the inhibition of 2 pathways of arachidonate metabolism may decrease infiltration of activated neutrophils in ischemic myocardium by attenuating chemotactic function of neutrophils, resulting in reduction of the extent of myocardial infarction.
为评估中性粒细胞和花生四烯酸代谢产物在心肌梗死进展中的作用，在犬心肌梗死90分钟闭塞/5小时再灌注模型中，研究了花生四烯酸代谢抑制剂对心肌损伤程度和中性粒细胞功能的影响。血栓素A2合成酶抑制剂CV - 4151和脂氧合酶抑制剂AA - 861可显著减小梗死面积。它们还减弱了趋化因子白三烯B4的产生以及从外周循环分离的中性粒细胞的趋化活性。在这些条件下，外周白细胞计数的增加和缺血心肌中中性粒细胞的浸润均受到抑制。这些结果表明，抑制花生四烯酸代谢的两条途径可能通过减弱中性粒细胞的趋化功能，减少活化中性粒细胞在缺血心肌中的浸润，从而降低心肌梗死的程度。
