Effects of propranolol administration on cardiac responses to burn injury

Previous studies showing that propranolol upregulates beta-adrenergic receptors and protects against myocardial ischemia led us to hypothesize that preburn propranolol would protect against postburn cardiac dysfunction. Guinea pigs were treated with propranolol 3 mg/kg/day for 14 days, then deeply anesthetized and subjected to a 45% 3 degrees scald burn; eight guinea pigs treated with propranolol served as the control group (group 1). Burned guinea pigs were resuscitated with Ringer's lactate given as either 4 ml (group 2, N = 8), 6 ml (group 3, N = 10), or 8 ml (group 4, N = 6) per kg/% burn. Guinea pigs treated for 14 days with vehicle (water) were subjected to either sham burn (non-propranolol control, group 5, N = 10) or burn and treatment (group 6, N = 10) as described for group 2. Fluid resuscitation in non-propranolol-treated guinea pigs failed to overcome burn-induced cardiac deficits, as indicated by significantly lower left ventricular pressure, 86 +/- 2 versus 62 +/- 3 mm Hg; +dP/dt max, 1365 +/- 43 versus 1110 +/- 44 mm Hg/sec; -dP/dt max, 1184 +/- 31 versus 881 +/- 40 mm Hg/sec, p < 0.001. Burn-mediated cardiac defects occurred in all propranolol-treated guinea pigs regardless of the fluid volume given. Our data show that (1) propranolol did not protect against burn-induced cardiac dysfunction, and (2) chronic beta-adrenergic blockade increases postburn fluid requirements for maintenance of cardiodynamic stability and for survival.