• Xian-Fei Ji, Shuo Wang, Lin Yang, and Chun-Sheng Li.
• Department of Emergency, Provincial Hospital Affiliated to Shandong University, Jinan, China.
• Resuscitation. 2012 May 1;83(5):640-4.

ObjectivePost-resuscitation myocardial dysfunction is a major cause of fatality in patients receiving successful cardiopulmonary resuscitation. The mechanism of post-resuscitation myocardial dysfunction is largely unknown, although is generally considered related to ischaemia occurring during cardiac arrest and resuscitation and/or reperfusion injury after restoration of circulation. A key mechanism responsible for reduced contractile reserves in chronic heart failure is impaired β-adrenergic receptor signalling. Thus, we hypothesised that β-adrenergic receptor signalling is markedly abnormal in the post-resuscitation period following cardiopulmonary resuscitation.MethodsMale landrace domestic pigs were randomised into a sham group (anaesthetised and instrumented, no ventricular fibrillation) or cardiopulmonary resuscitation (CPR) group (ventricular fibrillation) (n=8 per group). Haemodynamic and echocardiographic data were recorded. β-Adrenergic receptor signalling was assessed at 6h after the operation by measuring myocardial adenylate cyclase activity, β-adrenergic receptor density and β-adrenergic receptor kinase expression.ResultsLeft ventricular function in the CPR group was significantly decreased at 6 h after restoration of spontaneous circulation. Basal and isoproterenol-stimulated adenylate cyclase activity was blunted in the CPR group compared with the sham group. Total β-AR density was significantly decreased in CPR group compared with the sham group. Myocardial β-adrenergic receptor kinase expression was 2.03-fold greater in the CPR group than in the sham group.Conclusionsβ-Adrenergic receptor signalling is markedly impaired in the post-resuscitation period, which may be a mechanism of post-resuscitation myocardial dysfunction.Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

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