Department of Emergency and Disaster Medicine, Hamamatsu University School of Medicine, Hamamatsu City, Japan.
Shock. 2013 Jun;39(6):527-32. doi: 10.1097/SHK.0b013e318294e259.
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 °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 °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 °C during reperfusion. The U0126 group received U0126 (60 μM)-an extracellular signal-regulated kinase inhibitor-during reperfusion at 34 °C. The L-NIO (N-(1-iminoethyl)-L-ornithine dihydrochloride) group received L-NIO (2 μM)-an endothelial nitric oxide synthase inhibitor-5 min before global ischemia at 37 °C to the end of reperfusion at 34 °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.
在这项研究中，我们旨在通过 34°C 的诱导性低温（IH）比较低质量和高质量心肺复苏（CPR）对心脏保护的影响，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这种心脏保护作用。在 Langendorff 灌注和三苯基四唑氯（TTC）染色后，评估了六组大鼠心脏（n = 6）的左心室梗死面积。对照组在 37°C 下进行 30 分钟的全局缺血，然后进行 10 分钟的模拟低质量或高质量 CPR 再灌注和 90 分钟的 75mmHg 再灌注。IH 组在再灌注期间进行 IH 至 34°C。U0126 组在 34°C 再灌注期间接受 U0126（60μM）-细胞外信号调节激酶抑制剂。L-NIO（N-（1-亚氨基乙基）-L-鸟氨酸二盐酸盐）组在 37°C 下进行全局缺血前 5 分钟至再灌注至 34°C 结束时接受 L-NIO（2μM）-内皮型一氧化氮合酶抑制剂。低质量 CPR 组的对照组和 IH 组之间的梗死面积没有显著差异。然而，高质量 CPR 与 IH 联合可将梗死面积从 47.2%±10.2%降低至 26.0%±9.4%（P=0.005）。U0126 逆转了 IH 诱导的心脏保护作用（45.9%±9.4%，P=0.010），而 L-NIO 则没有显著影响。CPR 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 IH 诱导的心脏保护作用。
