Epinephrine and left ventricular function in humans: effects of beta-1 vs nonselective beta-blockade.

Abstract

Changes in cardiac performance in response to epinephrine administered by graded infusion were assessed by M-mode echocardiography in normotensive healthy subjects after pretreatment with placebo, the beta 1-selective blocker atenolol, or the nonselective beta-blocker propranolol. Epinephrine alone increased heart rate and left ventricular end diastolic dimension and decreased left ventricular end systolic dimension. Left ventricular performance as assessed by fractional shortening and systolic blood pressure/end-systolic volume (P/V) ratio was also increased. Atenolol pretreatment did not significantly affect the increase in heart rate by epinephrine. However, atenolol did prevent the effects of epinephrine on left ventricular dimensions and left ventricular performance at the lower infusion rates and significantly blunted these effects at the highest infusion rate. After propranolol, epinephrine significantly decreased left ventricular end diastolic dimension despite decreasing heart rate and left ventricular emptying (associated with a high afterload). P/V ratio remained unchanged. These results indicate that beta 2-receptors may play a major role in the increase in heart rate caused by epinephrine. In contrast, epinephrine's positive inotropic effect appears to be mediated primarily via beta 1-receptors and, at higher concentrations, possibly also through beta 2-receptors. The pattern of changes in left ventricular end diastolic dimension suggests that epinephrine increases venous return via both beta 1- and beta 2-receptor stimulation and that alpha-receptor stimulation (epinephrine after propranolol) may actually decrease venous return.