QUALITY OF CARDIOPULMONARY RESUSCITATION AFFECTS CARDIOPROTECTION BY INDUCED HYPOTHERMIA AT 34°C AGAINST ISCHEMIA/REPERFUSION INJURY IN A RAT ISOLATED HEART MODEL
QUALITY OF CARDIOPULMONARY RESUSCITATION AFFECTS CARDIOPROTECTION BY INDUCED HYPOTHERMIA AT 34°C AGAINST ISCHEMIA/REPERFUSION INJURY IN A RAT ISOLATED HEART MODEL
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DOI：
10.1097/shk.0b013e318294e259
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发表时间：
2013-06-01
期刊：
影响因子：
3.1
通讯作者：
Sato, Shigehito
中科院分区：
文献类型：
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作者：
Mochizuki, Toshiaki;Jiang, Qiliang;Sato, Shigehito
在这项研究中，我们旨在比较低质量和高质量心肺复苏(CPR)对34℃诱导低温(IH)心脏保护的影响，并检查细胞外信号调节激酶或内皮型一氧化氮合酶是否介导了这种心脏保护。在6只大鼠心脏上，用Langendorff灌流和氯化三苯基四氮唑染色评价左室梗死范围。对照组在37℃下进行30分钟的全脑缺血，然后进行10分钟的模拟低质量或高质量心肺复苏再灌注，以及在75毫米汞柱下进行90分钟的再灌注。在再灌流期间，IH组在34℃进行IH。L组在37℃全脑缺血前5min至34℃再灌流结束时给予内皮型一氧化氮合酶抑制剂L-NIO(N-5-(1-亚氨基乙基)-L-鸟氨酸二盐酸盐)。而采用高质量心肺复苏的IH组，脑梗塞面积由47.2%±10.2%降至26.0%+/-9.4%(P=0.005)。U0126逆转了IH诱导的心肌保护作用(45.9%+/-9.4%，P=0.010)，而L-NIO无明显作用。心肺复苏质量影响IH诱导的心脏保护作用。细胞外信号调节激酶可能介导了IH诱导的心肌保护作用。
In this study, we aimed to compare the effects of low-and high-quality cardiopulmonary resuscitation (CPR) on cardioprotection by induced hypothermia (IH) at 34 degrees C and examine whether extracellular signal-regulated kinase or endothelial nitric oxide synthase mediates this cardioprotection. Left ventricle infarct sizes were evaluated in six groups of rat hearts (n = 6) following Langendorff perfusion and triphenyltetrazolium chloride staining. Controls underwent 30 min of global ischemia at 37 degrees C, followed by 10 min of simulated low-or high-quality CPR reperfusion and 90 min of reperfusion at 75 mmHg. The IH groups underwent IH at 34 degrees C during reperfusion. The U0126 group received U0126 (60 mu M)-an extracellular signal-regulated kinase inhibitor-during reperfusion at 34 degrees C. The L-NIO (N-5-(1-iminoethyl)-L-ornithine dihydrochloride) group received L-NIO (2 mu M)-an endothelial nitric oxide synthase inhibitor-5 min before global ischemia at 37 degrees C to the end of reperfusion at 34 degrees C. Infarct size did not significantly differ between the control and IH groups receiving low-quality CPR. However, IH with high-quality CPR reduced the infarct size from 47.2% +/- 10.2% to 26.0% +/- 9.4% (P = 0.005). U0126 reversed the IH-induced cardioprotection (45.9% +/- 9.4%, P = 0.010), whereas L-NIO had no significant effect. Cardiopulmonary resuscitation quality affects IH-induced cardioprotection. Extracellular signal-regulated kinase may mediate IH-induced cardioprotection.