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Abstract

Introduction: The detrimental effects of epinephrine are closely related to its β- and a1- action, which significantly increases the severity of post-resuscitation (PR) myocardial dysfunction. In the present study, we investigated the effects of β- and β- plus α1- adrenergic blocking agents on post-resuscitation myocardial dysfunction and myocardial injury biomarkers. Methods: Twenty-four male Sprague-Dawley rats weighing between 450 - 550g were randomized into 4 groups: 1) placebo; 2) epinephrine; 3) epinephrine with β- blocker (propranolol) and; 4) epinephrine with β- plus α1- blockers (propranolol and prazosin). Ventricular fibrillation (VF) was electrically induced. CPR was initiated after 8 mins of untreated VF and continued for 8 mins. Defibrillation was then attempted. Ejection fraction (EF) and myocardial performance index (MPI) were measured at baseline and at hourly intervals for 4 hrs after resuscitation. Troponin I (Tn I) and N-terminal pro-brain natriuretic peptide (NT-pro BNP) were measured at baseline and at 1 and 4 hrs after resuscitation by the ELISA kits. Results: The β- and β- plus α1- blockers significantly reduced the severity of PR myocardial dysfunction. EF and MPI were 60.23 ± 1.23 and 1.01 ± 0.06 in the β- blocker group and 63.63 ± 1.51 and 0.89 ± 0.03 in the β- plus α1- blockers treated group compared to 39.90 ± 2.60 and 1.34 ± 0.10 in the epinephrine treated group and 44.58 ± 4.57 and 1.25 ± 0.10 in the placebo group at PR 4 hrs (p<0.05). The β- and β- plus α1- blockers pretreatment also reduced the releases of Tn I and NT-pro BNP compared with the placebo and epinephrine groups at PR 4 hrs (2.4 ± 1.0 and 1.8 ± 0.6 vs. 8.2 ± 5.2 and 9.5 ± 6.9 ng/L, p<0.05; 153.7 ± 44.9 and 151.7 ± 24.3 vs. 241.8 ± 16.9 and 298.9 ± 118.5 ng/L, p<0.05). The β- and β- plus α1-blockers significantly improved the duration of survival (67.8 ± 10.2 and 72.0 ± 0 vs. 34.4 ± 34.6 and 22.8 ± 26.4 hrs, p<0.05). Conclusions: The β- and β- plus α1-blockers reduced the severity of PR myocardial dysfunction and attenuated release of myocardial injury biomarkers with improved duration of survival in a rat model of CPR.