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.