Action of thyrotropin-releasing hormone in experimental hemorrhagic shock--cardiovascular mechanism.

Thyrotropin-releasing hormone (TRH) could improve mean arterial pressure (MAP), myocardial contractile parameters (+/- dp/dtmax, Vpm and Vmax) and increase plasma epinephrine level significantly at 10 min after TRH administration in hemorrhagic shock rabbits, but the action of TRH on MAP and the myocardial contractility did not appear in rabbits pre-treated with reserpine (4 mg/kg, 24 h pre-treatment, i.v.). TRH had no effects on myocardial contractility and MAP at 20 and 30 min after administration to rabbits pre-treated with beta-adrenergic blocker propranolol (1 mg/kg, 1 h before TRH injection i.v.), but it did exert effects on these parameters in rabbits pre-treated with alpha-adrenergic blocker phenoxybenzamine. Experiments in vitro showed that, although TRH (10(-4) M/L) had no direct effect on heart, left atrium and aortic strip, it did potentiate the inotropic effects of isoprenaline and dopamine on the left atrium. These results suggested that antishock effect of TRH is related to adrenergic system. TRH stimulates sympathomedullary system to secrete epinephrine and sensitize the beta-receptors, but not alpha-receptors. Thus, TRH improves cardiac contractility, cardiac output and hemodynamics during hemorrhagic shock. The sensitization of the beta- and dopamine receptors played an important role in producing direct peripheral actions of TRH.