The beneficial effects of heat-shock for prolonged hypothermic storage

Heat-shock has been reported to induce tolerance for subsequent ischemia. We wished to determine whether thermal stress is protective for hypothermic storage. Three groups of Sprague-Dawley rats were studied (n = 8 per group). Control animals received routine care (CONT) while anaesthetized rats were either warmed to 42 degrees C for 20 min (HEAT) or maintained at room temperature (SHAM). Twenty-four hours later, hearts were mounted on a Langendorff apparatus with an intraventricular balloon. Hearts were then flushed and stored in UW solution for 8 hr at 0 degrees C and reperfused for 45 min. Data are reported as a percentage of the prestorage results or as the absolute value (mean +/- SD). Recovery of developed pressure was significantly greater (P < 0.05) in the heat-shocked animals (79.5 +/- 10.2%) than in the SHAM (63.6 +/- 17.2%) or CONT groups (59.0 +/- 10.8%). Coronary flow was similarly enhanced (P < 0.05) in the HEAT group (86.8 +/- 5.5%) vs the CONT (77.0 +/- 12.3%) or SHAM hearts (74.5 +/- 10.2%). Diastolic compliance as assessed by evaluation of the end-diastolic pressure-volume curves was reduced in all groups (P < 0.0001) but not different among groups. Cardiac creatine kinase release during reperfusion was greater in the CONT and SHAM groups (CONT: 726.9 +/- 297.8 IU/g; SHAM: 548.9 +/- 420.9 IU/g) than in the heat-shocked rodents (282.3 +/- 175.5 IU/g, P < 0.05 HEAT vs CONT). Cardiac biopsies were performed sequentially in separate animals (n = 6 per group). Tissue levels of ATP and total adenine nucleotides were greater in the heat-shocked or SHAM hearts following reperfusion compared with controls (P < 0.05). Thermal stress provides additional protection for prolonged hypothermic storage.