Nonselective beta-blocking agent improves the outcome of cardiopulmonary resuscitation in a rat model

Postresuscitation myocardial dysfunction has been recognized as a leading cause of early death after initial successful resuscitation. Recent experimental and clinical studies have indicated that the beta-adrenergic effect of epinephrine significantly increases the severity of postresuscitation myocardial dysfunction. The fact that beta-adrenergic stimulation increases myocardial oxygen consumption during ventricular fibrillation is an important implication with respect to both the exogenous in terms of pharmacologic interventions during cardiopulmonary resuscitation and the endogenous as the result of intense sympathetic activation of cardiovascular collapse. Earlier experimental evidence has indicated that oxygenation improved by beta-blockade and beta1-blocking agent did offset the adverse effect of epinephrine. This prompted us to investigate the effect of beta-blockade on both exogenous and endogenous beta stimulation in an established rat model.

Prospective, randomized, controlled study.

Animal research laboratory.

Male Sprague-Dawley rats.

In this series of studies, propranolol was administrated before ventricular fibrillation as a pretreatment combined with epinephrine treatment during precordial compression and then alone in a prolonged cardiac arrest setting.

Improved postresuscitation myocardial dysfunction (cardiac index, dP/dt40, -dP/dt) was observed with propranolol, a nonselective beta-adrenergic blocker, in pretreated animals such that the beneficial effects were associated with better postresuscitation survival.

Nonselective beta-blockade improved the outcome of cardiopulmonary resuscitation in a rat model and deserves further evaluation in settings of cardiopulmonary resuscitation.