Effect of HEMADO on Level of CK-MB and LDH Enzymes after Ischemia/Reperfusion Injury in Isolated Rat Heart
Effect of HEMADO on Level of CK-MB and LDH Enzymes after Ischemia/Reperfusion Injury in Isolated Rat Heart
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DOI：
10.5681/bi.2013.003
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发表时间：
2013-01-01
期刊：
影响因子：
2.6
通讯作者：
Zaman, Jalal
中科院分区：
文献类型：
--
作者：
Amani, Mohammad;Jeddi, Sajad;Zaman, Jalal
简介：缺血/再灌注损伤主要引起心肌细胞损伤相关酶的升高，包括肌酸激酶同工酶（CK-MB）和乳酸脱氢酶（LDH）。CK-MB同工酶和LDH从心肌组织渗漏到血液中是急性心肌梗死的指标。本研究的目的是评估HEMADO对大鼠心脏IR损伤的影响及其与线粒体ATP敏感性K+通道（mitoKATP）的关系。研究方法：雄性Wistar大鼠28只，体重250- 300 g，随机分为4组（每组7只）：对照组（无缺血）、缺血再灌注组（有缺血+无HEMADO）、缺血再灌注组（HEMADO）、缺血再灌注组（HEMADO+5-HD）。将动物麻醉，并迅速取出心脏，安装在Langendorff装置上，并在37 ℃的恒定压力和温度下用Krebs-Henseleit溶液灌注。稳定20分钟后，缺血组暴露于40分钟的全脑缺血和连续90分钟的再灌注。结果：缺血再灌注损伤后5 min内冠脉血LDH、CK-MB水平明显升高。HEMADO降低酶的水平，使用5-HD消除HEMADO的作用。结论：HEMADO对心肌缺血再灌注损伤具有保护作用，其机制可能与降低心肌细胞CK-MB和LDH水平有关。HEMADO的心脏保护作用可能部分由mitoKATP介导。
Introduction: Ischemia/Reperfusion (IR) injury mainly causes the increase of enzymes involved in myocytes injury including CK-MB (creatine kinase-MB) isoenzyme and LDH (lactate dehydrogenase). Leakage of CK-MB isoenzyme and LDH from myocardial tissues to blood is indicator of acute myocardial infarction. The aim of this study was to assess the effect of HEMADO on IR injury and its relationship with mitochondrial ATP-sensitive K+ channels (mitoKATP) in rat heart. Methods: Twenty eight male Wistar rats (250-300g) were divided into four groups (seven members in each group): control (without ischemia), I/R (with ischemia+ without HEMADO), ischemia received HEMADO (HEMADO), ischemia received HEMADO and 5-HD (5-hydroxydecanoate, specific mitoKATP channel blocker) (HEMADO+5-HD). The animals were anesthetized and the hearts were quickly removed and mounted on Langendorff apparatus and perfused by Krebs-Henseleit solution under constant pressure and temperature of 37 degrees C. After 20 minutes of stabilization, ischemic groups were exposed to 40 minutes of global ischemia and consecutive 90 minutes of reperfusion. Results: IR injury increased the level of LDH and CK-MB in the collected coronary flow during 5 minutes since start of reperfusion. HEMADO reduced the enzymes' levels and using 5-HD abolished the effect of HEMADO. Conclusion: Our findings indicated that HEMADO could protect the heart against ischemia-reperfusion injury by decreasing the CK-MB and LDH levels. The cardioprotective effect of HEMADO may be mediated in part by mitoKATP.