[离体心脏缺血再灌注下线粒体通透性转换孔开放敏感性的非依赖性调节]

[No-dependent modulation of the sensitivity of the mitochondrial permeability transition pore opening under ischemia-reperfusion of the isolated heart].

作者信息

Shimanskaia T V, Dobrovol'skiĭ F V, vavilova G L, Strutinskaia N A, Rudyk E V, Sagach V F

出版信息

Ross Fiziol Zh Im I M Sechenova. 2009 Jan;95(1):28-37.

PMID:19323441

Abstract

The role of nitric oxide (NO) in modulation of sensitivity ofmitochondnal permeability transition pore (MPTP) opening under exposure to calcium as inductor was studied in experiments on the isolated heart (on Langendorff) and isolated mitochondria. The MPTP opening was studied on the hearts under ischemia-reperfusion and of the mitochondrial calcium loading. We investigated the degree ofreperfusional injury of the heart functional state after preliminary administration of the classic inhibitor of MPTP opening: cyclosporin A, the nitroprussid sodium salt as NO donor, NO-synthase (NOS) inhibitors such as L-NMMA and aminoguanidin to perfusional solution, and also the influence of Ca+ in the range of concentrations (10(-8)-10(-4) M) on the mitochondrial swelling under its preincubation with L-NMMA (10(-4) M). It is shown that the protective effect of nitric oxide on myocardium under reperfusion of ischemic heart will be realised by means of the inhibiting of Ca2+ -induced MPTP opening.

摘要

在离体心脏（Langendorff 装置）和离体线粒体实验中，研究了一氧化氮（NO）在以钙为诱导剂暴露条件下对线粒体通透性转换孔（MPTP）开放敏感性的调节作用。在缺血再灌注心脏和线粒体钙负荷条件下研究了 MPTP 的开放情况。我们研究了预先给予经典的 MPTP 开放抑制剂环孢素 A、硝普钠作为 NO 供体、L-NMMA 和氨基胍等 NO 合酶（NOS）抑制剂至灌注液后，心脏功能状态的再灌注损伤程度，以及在浓度范围为（10⁻⁸ - 10⁻⁴ M）的 Ca²⁺ 与 L-NMMA（10⁻⁴ M）预孵育后对线粒体肿胀的影响。结果表明，一氧化氮对缺血心脏再灌注时心肌的保护作用将通过抑制 Ca²⁺ 诱导的 MPTP 开放来实现。