Heat pretreatment differentially affects cardiac fatty acid accumulation during ischemia and postischemic reperfusion

We investigated whether the cardioprotection induced by heat stress (HS) pr etreatment is associated with mitigation of phospholipid degradation during the ischemic and/or postischemic period. The hearts, isolated from control rats and from heat-pretreated rats (42 degreesC for 15 min) either 30 min (HS0.5-h) or 24 h (HS24-h) earlier, were subjected to 45 min of no-flow isc hemia, followed by 45 min of reperfusion. Unesterified arachidonic acid (AA ) accumulation was taken as a measure for phospholipid degradation. Signifi cantly improved postischemic ventricular functional recovery was only found in the HS24-h group. During ischemia, AA accumulated comparably in control and both HS groups. During reperfusion in control and HS0.5-h hearts, AA f urther accumulated (control hearts from 82 +/- 33 to 109 +/- 51 nmol/g dry wt, not significant; HS-0.5h hearts from 52 +/- 22 to 120 +/- 53 nmol/g dry wt; P< 0.05). In contrast, AA was lower at the end of the reperfusion phas e in HS24-h hearts than at the end of the preceding ischemic period (74 +/- 18 vs. 46 +/- 23 nmol/g dry wt; P< 0.05). Thus accelerated reperfusion-ind uced degradation of phospholipids in control hearts is completely absent in HS24-h hearts. Furthermore, the lack of functional improvement in HS0.5-h hearts is also associated with a lack of beneficial effect on lipid homeost asis. Therefore, it is proposed that enhanced membrane stability during rep erfusion is a key mediator in the heat-induced cardioprotection.