ACUTE L-TRIIODOTHYRONINE ADMINISTRATION POTENTIATES INOTROPIC RESPONSES TO BETA-ADRENERGIC STIMULATION IN THE ISOLATED-PERFUSED RAT-HEART

Objective: Acute inotropic effects of triiodothyronine (T3) have been reported, employing both in vivo experimental animal models and in vit ro isolated heart perfusions. However, the mechanisms responsible for these acute inotropic effects remain unclear. The aim of this study, t herefore, was to delineate the role of the beta-adrenergic receptor sy stem in these acute responses, Methods: The hearts from both euthyroid and hypothyroid (treated with 0.05% PTU in drinking water) male Sprag ue-Dawley rats were used in 5 experimental study protocols. Hearts fro m euthyroid rats were perfused with buffer containing either T3 (10(-7 ) M) or control while continuously recording left ventricular function for 10 min ('acute effects'). Two-hour perfusions ('subacute effects' ) and cardiac responses following increasing doses of isoproterenol (1 0(-10) to 10(-6) M) in the presence or absence of T3-containing buffer (acute interaction) were also determined. In hypothyroid rats, the su bacute responses and the acute interactions were investigated. Results : In the presence of T3. an acute, significant potentiation of the ino tropic responses following beta-adrenergic stimulation with isoprotere nol was observed in both rat cohorts, which was more pronounced in hea rts from euthyroid rats. An acute ( < 40 s), but transient (79 +/- 8 s ), direct inotropic response was observed in hearts from euthyroid rat s. No cardiac responses were seen during a 2-h perfusion in hearts fro m either euthyroid or hypothyroid rats. Conclusions: The acute inotrop ic effects of T3 In non-ischemic myocardium probably result from an ac ute interaction between T3 and catecholamines rather than through a di rect inotropic effect of T3 alone.