Attenuation by Heat Stress of a Submaximal Calcium Paradox in the Rabbit Heart

Heat stress limits the injury associated with myocardial ischaemia and reperfusion, an effect previously attributed to enhanced endogenous anti-oxidant activity. We examined the influence of heat stress on the calcium paradox, and injury in which oxidant stress in not thought to play a major role. Twenty-four hours following sham or true heat stress, rabbits were re-anaesthetized and hearts either removed for stress protein analysis (n = 8), or Langendorff-perfused (n = 20) and subjected to a calcium paradox. Ten minutes following calcium repletion (Ca2+ = 1.3 mM), left ventricular developed pressure was better preserved in heat stress vs control hearts (38.3 ± 5.0 vs 18.8 ± 4.1 mmHg, respectively, P = 0.003) whilst contracture, measured by left ventricular enddiastolic pressure, was diminished (21.6 ± 4.7 vs 39.9 ± 5.2 mmHg, respectively, P = 0.02). Creatine phosphokinase release at 1 min was less in heat stress vs control hearts (10.6 ± 8.6 vs 86.4 ± 33.7 U/min/g, respectively, P = 0.01). The myocardial content of the 72 kDa stress protein was elevated eight-fold in heat stress vs control hearts (2.8 ± 0.02 vs 0.4 ± 0.1 U, respectively, P = 0.01), This study suggest that some portion of the stress protein response represents a form of cardiac adaptation capable of limiting myocyte injury independent of anti-oxidant mechanisms.