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钾通道激活剂与一氧化氮供体在大鼠长期给药及饮食诱导代谢综合征条件下的梗死限制疗效

Infarct-Limiting Efficacy of K Channel Activators and Nitric Oxide Donors under Conditions of Their Chronic Administration and Diet-Induced Metabolic Syndrome Conditions in Rats.

作者信息

Naryzhnaya N V, Mukhomedzyanov A V, Kilin M, Voronkov N S, Kurbatov B K, Maslov L N

机构信息

Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.

出版信息

Bull Exp Biol Med. 2025 May;179(1):1-5. doi: 10.1007/s10517-025-06421-y. Epub 2025 Jul 18.

Abstract

Coronary occlusion (45 min) and reperfusion (2 h) were modeled, and the ratio of the necrosis area to area at risk ratio was measured in rats. Metabolic syndrome was induced by high-carbohydrate high-fat diet for 84 days. A single administration of diazoxide, nicorandil at a dose of 5 mg/kg or nitroglycerin at a dose of 0.24 mg/kg to animals without metabolic syndrome resulted in a decrease in infarct size. A 21-day course of diazoxide had no infarct-limiting effect. After course administration of nicorandil or nitroglycerin, we observed a trend toward a decrease in infarct size, which completely disappeared 2 weeks after the course of therapy. In rats with metabolic syndrome, no infarct-limiting effect of diazoxide, nicorandil, and nitroglycerin was revealed.

摘要

建立冠状动脉闭塞(45分钟)和再灌注(2小时)模型,并在大鼠中测量坏死面积与危险面积的比值。通过高碳水化合物高脂肪饮食84天诱导代谢综合征。对无代谢综合征的动物单次给予二氮嗪、5mg/kg剂量的尼可地尔或0.24mg/kg剂量的硝酸甘油可使梗死面积减小。二氮嗪21天疗程无梗死限制作用。尼可地尔或硝酸甘油疗程给药后,我们观察到梗死面积有减小趋势,但在疗程结束2周后这种趋势完全消失。在患有代谢综合征的大鼠中,未发现二氮嗪、尼可地尔和硝酸甘油有梗死限制作用。

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