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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Effects of ATP-sensitive potassium channel blockers on vascular hyporeactivity, mesenteric blood flow, and survival in lipopolysaccharide-induced septic shock model
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Effects of ATP-sensitive potassium channel blockers on vascular hyporeactivity, mesenteric blood flow, and survival in lipopolysaccharide-induced septic shock model

机译：ATP敏感性钾通道阻滞剂对脂多糖诱导的败血性休克模型中血管反应性低，肠系膜血流量和存活的影响

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摘要

In this study, the possible therapeutic effects of various ATP-sensitive potassium channel (KATP) blockers (glibenclamide, repaglinide, 5-HD, HMR-1098) have been tested in experimental septic shock model. Rats were given lipopolysaccharide (1 mg.kg(-1)) to create experimental shock model and 4 h later, under 400 mg.kg(-1) chloral hydrate anesthesia, parameters such as blood pressure, mesenteric blood flow, the response of mesenteric circulation to phenylephrine (vasoconstrictor stimulation), and organ and oxidative damage were analyzed. Also 75 mg.kg(-1) lethal dose of lipopolysaccharide was given to mice and effects of KATP blockers on survival have been tested. Non-selective blocker glibenclamide with sulphonylurea structure and sarcolemmal KATP channel blocker HMR-1098, which have the similar chemical structure, have improved the pathological parameters such as decrease in mesenteric blood flow, vascular hyporeactivity, but could not prevent the decrease in blood pressure, and oxidative and organ damage that were observed in the shock model. Also, both blockers have decreased the mortality rate from 80% to 40%-50%. Similar (preventive) therapeutic effects were not observed with non-selective blocker repaglinide and mitochondrial KATP channel blocker 5-HD, which were non-sulphonylurea structure. As a result, only KATP channel blockers that have sulphonylurea structure can be a new therapeutic approach in septic shock.
机译：在这项研究中，已在实验性败血性休克模型中测试了各种ATP敏感性钾通道（KATP）阻断剂（格列本脲，瑞格列奈，5-HD，HMR-1098）的可能治疗作用。给大鼠脂多糖（1 mg.kg（-1））建立实验性休克模型，并于4 h后在400 mg.kg（-1）水合氯醛麻醉下，测定血压，肠系膜血流，分析了去氧肾上腺素的肠系膜循环（血管收缩剂刺激）以及器官和氧化损伤。还向小鼠给予了75 mg.kg（-1）致死剂量的脂多糖，并测试了KATP阻断剂对存活的影响。具有相似化学结构的具有磺酰脲结构的非选择性阻滞剂格列本脲和肌膜KATP通道阻滞剂HMR-1098具有改善的病理学参数，例如肠系膜血流量减少，血管反应性降低，但不能防止血压下降，以及在休克模型中观察到的氧化和器官损伤。而且，两种阻滞剂都将死亡率从80％降低到40％-50％。非选择性阻滞剂瑞格列奈和线粒体KATP通道阻滞剂5-HD未观察到类似的（预防性）治疗作用，它们均为非磺酰脲结构。结果，只有具有磺酰脲结构的KATP通道阻滞剂才能成为败血性休克的新治疗方法。

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