β-receptor blocker influences return of spontaneous circulation and chemical examination in rats during cardiopulmonary resuscitation

Abstract

Abstract:Objective: We investigated the influence of β-receptor blocker metoprolol on return of spontaneous circulation (ROSC) during cardiopulmonary resuscitation (CPR) in rats with induced myocardial infarction (MI). Methods: Male Sprague-Dawley rats were randomly divided into three groups: the sham-operated group, the MI group without metoprolol, which was fed the vehicle, and the MI+metoprolol group receiving intragastric metoprolol. Each group was further divided randomly into three subgroups, depending on the dosage of epinephrine administered during subsequent CPR applied after the induction of asphyxial cardiac arrest. Results: The ROSC rate was significantly decreased in the low dose subgroup of MI group, unchanged in the medium dose subgroup of MI group, and significantly decreased in the high dose subgroup of MI group, compared with the same dose subgroup of sham-operated group. MI+metoprolol group had a lower ROSC rate than MI group in the medium dose subgroup, and a higher ROSC rate than MI group in the high dose subgroup. There was no difference in blood K + values of successful rats between MI group and MI+metoprolol group. The rats with successful CPR had lower blood K + values than rats with unsuccessful CPR in each of the three treatment groups. Conclusions: Metoprolol administered to MI rats over a long period significantly improved ROSC rates under an appropriate dose of epinephrine during CPR. An increasing high blood K + value would attenuate the rate of a successful CPR.

Immune recovery after fluid resuscitation in rats with severe hemorrhagic shock

“…The purpose of this study was to compare the effects of three resuscitation fluids on immune cell regulation in the early stage of hemorrhagic shock. Specifically, we evaluated the proportion of regulatory T cells (Tregs), which help maintain immune balance, and can limit inflammatory tissue damage caused by infection, autoimmunity, allogeneic immune responses, and antitumor immunity (Belkaid and Rouse, 2005;Zhao et al, 2013); we also evaluated the ratios of helper T (Th) and cytotoxic T (Tc), which can execute many crucial immune functions (Marcu et al, 2007;Zhang et al, 2008;Chen et al, 2014).…”