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ATP 敏感性钾通道表达增加可改善兔心右心室对缺氧的耐受能力。

Increased Expression of ATP-sensitive K Channels Improves the Right Ventricular Tolerance to Hypoxia in Rabbit Hearts.

机构信息

National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Inje University, Busan 614-735, Korea.

出版信息

Korean J Physiol Pharmacol. 2011 Aug;15(4):189-94. doi: 10.4196/kjpp.2011.15.4.189. Epub 2011 Aug 31.

Abstract

ATP-sensitive K(+) channels (K(ATP)) are major component of preventing ischemia-reperfusion injury. However, there is little information regarding to the expressional difference of K(ATP) and its function between left and right ventricles. In this study, we measured the lactate dehydrogenase release of rabbit heart slices in vitro and determined the difference of the K(ATP) expression at the both ventricles by measuring the level of K(ATP)-forming Kir6.2 (OcKir6.2) mRNA using in situ hybridization. The hearts were preconditioned with 15 min hypoxia and reoxygenated for 15 min before a hypoxic period of 60 min, followed by reoxygenation for 180 min. With hypoxic preconditioning (100% N(2)) with 15 min, left ventricles (LV) showed higher release of LDH comparing with right ventricles (RV). Adding K(ATP) blocker glibenclamide (10 µM) prior to a hypoxic period of 60 min, hypoxic preconditioning effect of RV was more abolished than LV. With in situ hybridization, the optical density of OcKir6.2 was higher in RV. Therefore, we suggest that different K(ATP) expression between LV and RV is responsible for the different response to hypoxia and hypoxic preconditioning of rabbit hearts.

摘要

三磷酸腺苷敏感性钾(K(ATP))通道是防止缺血再灌注损伤的主要组成部分。然而,关于左、右心室之间 K(ATP)的表达差异及其功能,信息很少。在这项研究中,我们通过原位杂交测量 K(ATP)形成 Kir6.2(OcKir6.2)mRNA 的水平,测量了兔心切片在体外的乳酸脱氢酶释放,并确定了 K(ATP)表达在左右心室的差异。在 60 分钟的缺氧期之前,心脏用 15 分钟的缺氧预处理并用 15 分钟再氧合,然后再氧合 180 分钟。用 15 分钟的缺氧预处理(100% N(2)),左心室(LV)与右心室(RV)相比,释放出更高的 LDH。在 60 分钟的缺氧期之前加入 K(ATP)阻断剂格列本脲(10 μM),RV 的缺氧预处理效果比 LV 更被抑制。通过原位杂交,OcKir6.2 的光密度在 RV 中更高。因此,我们认为 LV 和 RV 之间不同的 K(ATP)表达是导致兔心对缺氧和缺氧预处理的不同反应的原因。

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