Previous studies showing that propranolol upregulates p-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° scald burn; eight guinea pigs treated with propranolol served as the control group (group 1). Burned guinea pigs were resuscitated with Ringer's lactatc 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 diat (1) propranolol did not protect against burn-induced cardiac dysfunction, and (2) chronic p-adrenergic blockade increases postburn fluid requirements for maintenance of cardiodynamic stability and for survival.