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

• Published in: American journal of physiology. Heart and circulatory physiology Vol. 280; no. 4; pp. H1736 - H1743
• Main Authors: Cornelussen, Richard N. M, Van Der Vusse, Ger J, Roemen, Theo H. M, Snoeckx, Luc H. E. H
• Format: Journal Article
• Language: English
• Published: United States 01.04.2001
• Subjects: Animals; Arachidonic Acid - metabolism; Biomarkers - analysis; Creatine Kinase - blood; Fatty Acids, Nonesterified - metabolism; Heat Stress Disorders; HSP70 Heat-Shock Proteins - metabolism; In Vitro Techniques; Male; Myocardial Ischemia - metabolism; Myocardial Ischemia - physiopathology; Myocardial Reperfusion; Myocardial Reperfusion Injury - metabolism; Myocardial Reperfusion Injury - physiopathology; Myocardial Reperfusion Injury - prevention & control; Myocardium - metabolism; Rats; Rats, Inbred Lew; Reference Values; Ventricular Function, Left
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.2001.280.4.H1736

Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, 6200 MD Maastricht, The Netherlands We investigated whether the cardioprotection induced by heat stress (HS) pretreatment 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°C for 15 min) either 30 min (HS0.5-h) or 24 h (HS24-h) earlier, were subjected to 45 min of no-flow ischemia, followed by 45 min of reperfusion. Unesterified arachidonic acid (AA) accumulation was taken as a measure for phospholipid degradation. Significantly 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 further 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 phase 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-induced 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 homeostasis. Therefore, it is proposed that enhanced membrane stability during reperfusion is a key mediator in the heat-induced cardioprotection. heat shock proteins; lipid metabolism; cardioprotection; enzyme release