Propranolol decreases sympathetic nervous activity reflected by plasma catecholamines during evolution of myocardial infarction in man.

Plasma 1-norepinephrine and epinephrine contents were strikingly elevated in 70 patients during evolution of myocardial infarction. Propranolol or placebo, 0.1 mg/kg i.v., was administered randomly an average of 10 h after infarction and continued orally for 3 d. Propranolol, but not placebo, acutely decreased 1-norepinephrine contents from 2.24 +/- 1.33 (mean +/- SD) to 1.31 +/- 0.74 microgram/liter, P less than 0.001, and epinephrine contents from 0.97 +/- 0.42 to 0.74 +/- 0.42 microgram/liter, P less than 0.02. Decreases in 1-norepinephrine contents were related to the initial plasma concentrations, r = 0.85, P less than 0.001. A similar, but less strong relationship was observed between the initial epinephrine contents and propranolol-induced changes, r = -0.51, P less than 0.01. Propranolol reduced plasma-free fatty acid contents from 1,121 +/- 315 to 943 +/- 274 mumol/liter, P less than 0.001. Decreases in plasma contents of free fatty acids were related to decreases in epinephrine, r = 0.66, P less than 0.001. Propranolol did not cause significant additional changes in plasma catecholamine contents during the subsequent 3 d. In the placebo group 1-norepinephrine contents had decreased 24 h after infarction from 1.92 +/- 0.99 to 1.37 +/- 0.93 microgram/liter, P less than 0.02. Plasma epinephrine contents did not change. Heart rate remained below the control values during the entire study period in the propranolol, but increased in the placebo group. The data indicate that sympathetic hyperactivity, indirectly reflected by plasma catecholamine contents, is acutely reduced by propranolol during evolution of myocardial infarction.