HEAT-STRESS INDUCES RAPID RECOVERY OF MECHANICAL FUNCTION OF ISCHEMICFATTY-ACID PERFUSED HEARTS BY STIMULATING GLUCOSE-OXIDATION DURING REPERFUSION

Whole-body heat stress (HS) in rats leads to the accumulation of myoca rdial heat shock proteins and subsequent protection against ischemic i njury in glucose-perfused hearts. We determined whether HS treatment w ould confer protection against ischemia in hearts perfused with high l evels of fatty acids. In addition, since fatty acids can potentiate is chemic injury by inhibiting glucose metabolism, the effects of HS on g lucose utilization were also determined. Anesthetized rats were subjec ted to whole-body hyperthermia by raising body temperature to 41-42 de grees C for 15 min. Twenty-four hours later, their hearts were perfuse d with buffer containing either 11 mM glucose alone or 11 mM glucose a nd 1.2 mM palmitate, and then subjected to ischemic conditions followe d by reperfusion. In hearts perfused with glucose only, HS improved ao rtic flow (expressed as percent change from preischemic aortic flow) l ate into the reperfusion period. Rates of overall glucose utilization under these conditions were similar between control and IIS hearts. Wh en hearts were perfused with 1.2 mM palmitate, the benefits of HS on a ortic flow occurred at the onset of the reperfusion period. This benef icial effect was associated with a significant increase in glucose ox! dation. Our results show that HS induces a faster rate of recovery in fatty acid perfused hearts but does not offer more protection against ischemic damage when compared with hearts perfused with glucose as a s ole substrate.