一氧化氮合酶在急性和慢性适应常压低氧的梗死保护作用中的角色。
The Role of NO Synthase in the Infarct-Limiting Effect of Urgent and Chronic Adaptation to Normobaric Hypoxia.
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. 2023 Jan;174(3):304-307. doi: 10.1007/s10517-023-05696-3. Epub 2023 Feb 1.
We studied the role of NO synthase in the infarct-limiting effect of short-term (SNH) and chronic continuous normobaric hypoxia (CNH). In male Wistar rats, SNH (6 sessions of 10-min hypoxia 8% O2 and 10-min reoxygenation) or CNH (12% O2 for 21 days) was modeled. In 30 min after SNH or 24 h after CNH, the rats were subjected to coronary artery occlusion (45 min) and reperfusion (2 h). The following drugs were administered to rats: non-selective NO synthase inhibitor L-NAME (10 mg/kg), inhibitor of inducible NO synthase S-methylthiourea (3 mg/kg), and inhibitor of neuronal NO-synthase 7-nitroindazole (50 mg/kg). NO donor diethylenetriamine was administered intravenously in a dose 2 mg/kg. It was found that L-NAME and S-methylthiourea abolished the infarct-limiting effect of SNH and CNH. Diethylenetriamine increased cardiac tolerance to ischemia/reperfusion. It is believed that inducible NO synthase plays an important role in the cardioprotective effect of normobaric hypoxia.
我们研究了一氧化氮合酶（NOS）在短期（SNH）和慢性持续常压缺氧（CNH）的梗死限制效应中的作用。在雄性 Wistar 大鼠中，构建 SNH（6 次 10 分钟缺氧 8% O2 和 10 分钟复氧）或 CNH（12% O2 21 天）模型。在 SNH 后 30 分钟或 CNH 后 24 小时，大鼠进行冠状动脉闭塞（45 分钟）和再灌注（2 小时）。向大鼠给予以下药物：非选择性 NOS 抑制剂 L-NAME（10mg/kg）、诱导型 NOS 抑制剂 S-甲基硫脲（3mg/kg）和神经元 NOS 抑制剂 7-硝基吲唑（50mg/kg）。NO 供体二亚乙基三胺以 2mg/kg 的剂量静脉内给予。结果发现，L-NAME 和 S-甲基硫脲消除了 SNH 和 CNH 的梗死限制效应。二亚乙基三胺增加了心脏对缺血/再灌注的耐受性。据信，诱导型 NOS 在常压缺氧的心脏保护作用中发挥重要作用。
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