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Shen-Fu Injection (参附注射液) Alleviates Post-resuscitation Myocardial Dysfunction by Up-regulating Expression of Sarcoplasmic Reticulum Ca2+-ATPase
  
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KeyWord:epinephrine, Shen-fu Injection, sarcoplasmic reticulum Ca2+ ATPase 2a, cardiac arrest, cardiopulmonary resuscitation, Chinese medicine
Author NameAffiliationE-mail
GUO Zhi-jun, WU Cai-jun   
LI Chun-sheng Department of Emergency, Beijing Chaoyang Hospital, Capital Medical University, Beijing (100020), China lcscyyy@163.com 
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Abstract:
      Objective: To compare the effect of Shen-Fu Injection (SFI) and epinephrine on the expression of sarcoplasmic reticulum Ca2+ ATPase 2a (SERCA2a) in a pig model with post-resuscitation myocardial dysfunction. Methods: Ventricular fibrillation (VF) was electrically induced in Wu-zhi-shan miniature pigs. After 8 min of untreated VF and 2 min of cardiopulmonary resuscitation (CPR), all animals were randomly administered a bolus injection of saline placebo (SA group, n=10), SFI (0.8 mg/kg, SFI group, n=10) or epinephrine (20 μg/kg, EPI group, n=10). After 4 min of CPR, a 100-J shock was delivered. If the defibrillation attempt failed to attain restoration of spontaneous circulation (ROSC), manual chest compressions were rapidly resumed for a further 2 min followed by a second defibrillation attempt. Hemodynamic variables were recorded, and plasma concentrations of catecholamines were measured. Adenylate cyclase (AC), cyclic adenosine monophosphate (cAMP) and the expressions of β1-adrenoceptor (AR) and SERCA 2a were determined. Results: Cardiac output, left ventricular dp/dtmax and negative dp/dtmax were significantly higher in the SFI group than in the SA and EPI groups at 4 and 6 h after ROSC. The expression of β1-AR and SERCA2a at 24 h after ROSC were significantly higher in the SFI group than in the SA and EPI groups (P<0.05 or P<0.01). Conclusions: The administration of epinephrine during CPR decreased the expression of SERCA2a and aggravated postresuscitation myocardial function (P<0.01). SFI attenuated post-resuscitation myocardial dysfunction, and the mechanism might be related to the up-regulation of SERCA2a expression.
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