Jiang Cuicui, Xia Manli, Wang Min, Chen Shipiao
Jiaxing University College of Medicine, Jiaxing 314001, China.
Zhejiang Da Xue Xue Bao Yi Xue Ban. 2013 May;42(3):326-30.
To investigate the protective effect of dexmedetomidine (Dex) preconditioning against ischemia/reperfusion (I/R) injuries in isolated rat hearts and its relation to mitochondrial permeability transition pore (mPTP) and mitochondrial ATP-sensitive K(+) channel (mitoKATP).
The hearts of male SD rats were isolated to mount on the Langendorff apparatus and subjected to 30 min global ischemia followed by 120 min reperfusion. The isolated hearts were treated with Dex (10 nmol/L) before ischemia for 15 min. The left ventricular hemodynamic parameters,coronary flow (CF) and the lactate dehydrogenase (LDH) release in the coronary effluent at 5 min reperfusion were measured. The formazan content was assayed to determine the myocardial viability at the end of reperfusion.
Compared with normal controls, I/R markedly decreased the left ventricular developed pressure and CF during the whole reperfusion period and the formazan content; while the left ventricular end diastolic pressure and LDH release were significantly increased. Dex preconditioning markedly improved the myocardial viability and cardiac function (P<0.01), which were reversed by the treatment with both atractyloside (20 μmol/L before ischemia), an opener of mPTP, and 5-hydroxydecanoate (100 μmol/L at the beginning of reperfusion), an inhibitor of mitoKATP, for 20 min.
Dex has protective effect against I/R injuries in isolated rat hearts, which may be related to inhibiting the opening of mPTP at the beginning of reperfusion and activating mitoKATP before ischemia.
探讨右美托咪定（Dex）预处理对离体大鼠心脏缺血/再灌注（I/R）损伤的保护作用及其与线粒体通透性转换孔（mPTP）和线粒体ATP敏感性钾通道（mitoKATP）的关系。
取雄性SD大鼠心脏，安装在Langendorff装置上，进行30分钟全心缺血，随后再灌注120分钟。在缺血前15分钟用Dex（10 nmol/L）处理离体心脏。测量再灌注5分钟时左心室血流动力学参数、冠脉流量（CF）及冠脉流出液中乳酸脱氢酶（LDH）的释放量。在再灌注结束时检测甲臜含量以确定心肌活力。
与正常对照组相比，I/R显著降低了整个再灌注期的左心室舒张末压和CF以及甲臜含量；而左心室舒张末压和LDH释放量显著增加。Dex预处理显著改善了心肌活力和心脏功能（P<0.01），用mPTP开放剂苍术苷（缺血前20 μmol/L）和mitoKATP抑制剂5-羟基癸酸（再灌注开始时100 μmol/L）处理20分钟可逆转这些作用。
Dex对离体大鼠心脏的I/R损伤具有保护作用，这可能与在再灌注开始时抑制mPTP开放以及在缺血前激活mitoKATP有关。
