RESUMO
<p><b>AIM</b>To investigate the effect of hypothalamic thyrotropin-releasing hormone (TRH) on cardiac function and its mechanism.</p><p><b>METHODS</b>The Sprague-Dawley rats were mounted in a stereotaxic apparatus and a guide cannula placed in the left hypophysiotropic area, through which TRH were microinjected in presence or absence of L-NAME and atropine. The left ventricular systolic pressure (LVSP), heart rate (HR) and the maximum velocity of ascending or descending in intraventricular pressure (+/- dp/dt(max)) were recorded.</p><p><b>RESULTS</b>(1) TRH microinjected into the hypophysiotropic area induced a significant increase of LVSP, HR, dp/dt and-dp/dt(max) (P < 0.05, P < 0.01). (2) L-NAME significant increased LVSP and pretreatment with L-NAME inhibited the positive effects induced by TRH. (3) Atropine increased LVSP and dp/dt(max) (P < 0.05), but it significantly descended heart rate (P < 0.05). Pretreatment with atropine weakened the tachycardiac response induced by TRH.</p><p><b>CONCLUSION</b>(1) Hypothalamic TRH can produce positive inotropic and chronotropic response to myocardium. (2) Hypothalamic endogenous NO can descend LVSP, but has no effects on HR, dp/dt(max), and-dp/dt(max). The effect of TRH is through nitric oxide-dependent pathway. (3) Hypothalamic endogenous cholinergic transmitter can produce negative chronotropic and positive inotropic response to myocardium. Hypothalamic TRH mediates cardiac function maybe partly through cholinergic M receptor.</p>