Shen-Fu injection reduces impaired myocardial β-adrenergic receptor signaling after cardiopulmonary resuscitation.
- Author:
Xian-fei JI
1
;
Hong-bin JI
;
De-ya SANG
;
Shuo WANG
;
Lin YANG
;
Chun-sheng LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cardiopulmonary Resuscitation; adverse effects; Drugs, Chinese Herbal; administration & dosage; therapeutic use; Male; Receptors, Adrenergic, beta; metabolism; Signal Transduction; drug effects; Swine
- From: Chinese Medical Journal 2013;126(4):697-702
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDPost-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.
METHODSVentricular 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 return 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.
RESULTSTreatment with SFI produced better maximum rate of left ventricular pressure increase (dp/dt(max)) and maximum rate of left ventricular pressure decline (-dp/dt(max)), cardiac output, and ejection fraction after ROSC. SFI treatment was also associated with lower myocardial β-adrenergic receptor kinase expression, whereas basal and isoproterenol-stimulated adenylate cyclase activity and the total β-AR density were significantly increased in the SFI group when compared with the placebo group.
CONCLUSIONSFI attenuated post-resuscitation myocardial dysfunction by preventing impaired myocardial β-AR signaling after CPR.