Thyrotropin-releasing hormone (TRH) improved mean arterial pressure (MAP) and 
myocardial contractility (dp/dtmax, -dp/dtmax, Vpm, and Vmax) and increased 
plasma epinephrine levels significantly at 10 min after TRH treatment in rabbits 
following shock, but the effects of TRH on MAP and myocardial contractility 
disappeared in reserpinized rabbits (4 mg/kg, 24 hr pre-treatment, iv). TRH had 
no effect on myocardial contractility and MAP at 20 and 30 min post-treatment in 
rabbits pre-treated with the beta adrenergic blocker propranolol (1 mg/kg, 1 hr 
before TRH treatment, iv), but the alpha adrenergic blocker phenoxybenzamine did 
not affect these responses to TRH. Experiments in vitro show that although TRH 
(10(-3) to 10(-8) M) had no direct effects on the isolated heart, left atrium, 
and aortic strip, it did potentiate the inotropic effects of isoprenaline and 
dopamine on the left atrium. These results suggest that the antishock effects of 
TRH are related to adrenergic systems, perhaps acting on the 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 adrenergic 
and dopamine receptors may play an important role in the direct peripheral 
cardiovascular mechanism of TRH effects.