Heat acclimation induces changes in cardiac mechanical performance: the role of thyroid hormone

The involvement of reduced thyroxine level in the emergence of heat acclima tion-induced negative lusitropic effect was examined. Experiments were card ed out on I)control rat hearts maintained at 24 +/- 1 degrees C (C); 2)rat hearts acclimated at 34 degrees C for 1 mo (AC); 3)AC-euthyroid rat hearts, via administration of thyroxine in the drinking water (AT); and 4) hypothy roid rat hearts, maintained at 24 +/- 1 degrees C, via administration of th iouracil in the drinking water (CP). Systolic pressure and velocities of co ntraction (dP/dt . P) and relaxation (- dP/dt . P) were measured using the Langendorff perfusion system. The steady-state levels of Ca2+-ATPase and ph ospholamban mRNAs and the expression of the encoded proteins Ca2+-ATPase (S ERCA) and phospholamban (PLB) were measured, using semi-quantitative RT-PCR and Westrern immunoblotting, respectively. Rat thyroxine levels were measu red using RIA. Heat acclimation, which brought about a reduced thyroxine le vel, led to downregulation of Ca(2+)ATPase mRNA expression and translation and upregulation of phospholamban mRNA and PLB. Consequently, the PLB-to-SE RCA ratio (PLB/SERCA) of the AC hearts showed a significant increase. These changes, as well as the greater pressure generation and the reduced dP/dt . P and -dP/dt . P observed in AC hearts were blunted in the AT hearts. Our data suggest that sustained heat acclimation-induced low thyroxine level h as a decisive effect on the contractile machinery of the AC heart. Elevated PLB/SERCA apparently explains the negative lusitropic effect observed in t hese hearts.