Impaired 尾-adrenergic receptor signalling in post-resuscitation myocardial dysfunction
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摘要

Objective

Post-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 尾-adrenergic receptor signalling. Thus, we hypothesised that 尾-adrenergic receptor signalling is markedly abnormal in the post-resuscitation period following cardiopulmonary resuscitation.

Methods

Male 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. 尾-Adrenergic receptor signalling was assessed at 6 h after the operation by measuring myocardial adenylate cyclase activity, 尾-adrenergic receptor density and 尾-adrenergic receptor kinase expression.

Results

Left 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 尾-AR density was significantly decreased in CPR group compared with the sham group. Myocardial 尾-adrenergic receptor kinase expression was 2.03-fold greater in the CPR group than in the sham group.

Conclusions

尾-Adrenergic receptor signalling is markedly impaired in the post-resuscitation period, which may be a mechanism of post-resuscitation myocardial dysfunction.

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