Quality of Cardiopulmonary Resuscitation Affects Cardioprotection by Induced Hypothermia at 34°C Against Ischemia/Reperfusion Injury in a Rat Isolated Heart Model

ABSTRACTIn 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.