| Autor: |
Xian-fei, Ji, Hong-bin, Ji, De-ya, Sang, Shuo, Wang, Lin, Yang, Chun-sheng, Li |
| Rok vydání: |
2013 |
| Předmět: |
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| Zdroj: |
Chinese medical journal. 126(4) |
| ISSN: |
2542-5641 |
| Popis: |
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.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 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.Treatment 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.SFI attenuated post-resuscitation myocardial dysfunction by preventing impaired myocardial β-AR signaling after CPR. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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