Shen-Fu injection reduces impaired myocardialβ-adrenergic receptor signaling after cardiopulmonary r

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Background Post-resuscitation myocardial dysfunction has been implicated as a major cause of fatal outcome in patients who survive initially successful cardiopulmonary resuscitation (CPR).In our previous study,we found that impaired myocardial β-adrenergic receptor (AR) signaling is a key mechanism in post-resuscitation myocardial dysfunction and Shen-Fu injection (SFI) can attenuate post-resuscitation myocardial dysfunction.However,whether SFI can prevent impaired post-resuscitation myocardial β-AR signaling is not yet known.In this study,we investigated the effect of SFI on impaired myocardial β-AR signaling occurring post-resuscitation in a porcine model of cardiac arrest.Methods Ventricular fibrillation was induced electrically in anesthetized male landrace domestic pigs.After 4 minutes of untreated ventricular fibrillation,cardiopulmonary resuscitation was initiated.Sixteen successfully resuscitated pigs were randomized to receive a continuous infusion of either SFI (0.5 ml/min; n=8) or saline (placebo; n=8) for 6 hours,beginning 15 minutes after the ret of spontaneous circulation (ROSC).Hemodynamic and echocardiographic data were recorded.β-AR signaling was assessed at 6 hours after the intervention by measuring myocardial adenylate cyclase activity,β-AR density and β-AR kinase expression.Results Treatment with SFI produced better maximum rate of left ventricular pressure increase (dp/dtrmax) and maximum rate of left ventricular pressure decline (-dp/dtmax),cardiac output,and ejection fraction after ROSC.SFI treatment was also associated with lower myocardial β-adrenergic receptor kinase expression,whereas basal and isoproterenolstimulated adenylate cyclase activity and the total β-AR density were significantly increased in the SFI group when compared with the placebo group.Conclusion SFI attenuated post-resuscitation myocardial dysfunction by preventing impaired myocardialβ-AR signaling after CPR.
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