Nicorandil Attenuates FeCl_3-Induced Thrombus Formation Through the Inhibition of Reactive Oxygen Species Production(Vascular Medicine)

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Background: Although nicorandil has a number of beneficial cardiovascular actions, its effects on endothelial cells in the context of thrombosis have not been elucidated. Methods and Results: Arterial thrombosis was induced by endothelial injury caused by FeCl_3 in the mouse testicular artery. Thrombus growth led to complete occlusion 12min after endothelial injury in control mice. The antiplatelet agent, tirofiban, and nicorandil significantly slowed the growth of thrombi, resulting in arterial occlusion after 58min and 55min, respectively. In the absence of endothelial cells, nicorandil did not inhibit platelet aggregation. Diazoxide and high-dose isosorbide dinitrate both showed a similar effect to that of nicorandil. The beneficial effect of nicorandil was prevented by 5-hydroxydecanoate, but not by L-NAME. The production of reactive oxygen species by FeCl_3 treatment was measured with the specific fluorescent probe, dihydrorhodamine 123. After FeCl_3 treatment, nicorandil significantly inhibited the increase in fluorescence. In further experiments, incubation of human umbilical vein endothelial cells with nicorandil did not change the endothelial nitric oxide synthase (eNOS) mRNA levels, eNOS phosphorylation or nitrite production. Conclusions: Nicorandil attenuates FeCl_3-induced thrombus formation in the mouse testicular artery, which suggests that it may inhibit the generation of reactive oxygen species by FeCl_3-treated endothelial cells through activation of the mitochondrial ATP-sensitive potassium channels.
社団法人日本循環器学会の論文
2009-02-20

Nicorandil Attenuates FeCl_3-Induced Thrombus Formation Through the Inhibition of Reactive Oxygen Species Production(Vascular Medicine)

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