Heat stress pretreatment mitigates postischemic arachidonic acid accumulation in rat heart.
Heat stress pretreatment of the heart is known to protect this organ against an ischemic/reperfusion insult 24 h later. Degradation of membrane phospholipids resulting in tissue accumulation of polyunsaturated fatty acids, such as arachidonic acid, is thought to play an important role in the multifactorial process of ischemia/reperfusion-induced damage. The present study was conducted to test the hypothesis that heat stress mitigates the postischemic accumulation of arachidonic acid in myocardial tissue, as a sign of enhanced membrane phospholipid degradation. The experiments were performed on hearts isolated from rats either 24 h after total body heat treatment (42 degrees C for 15 min) or 24 h after sham treatment (control). Hearts were made ischemic for 45 min and reperfused for another 45 min. Heat pretreatment resulted in a significant improvement of postischemic hemodynamic performance of the isolated rat hearts. The release of creatine kinase was reduced from 30 +/- 14 (control group) to 17 +/- 5 units/g wet wt per 45 min (heat-pretreated group) (p < or = 0.05). Moreover, the tissue content of the inducible heat stress protein HSP70 was found to be increased 3-fold 24 h after heat treatment. Preischemic tissue levels of arachidonic acid did not differ between heat-pretreated and control hearts. The postischemic ventricular content of arachidonic acid was found to be significantly reduced in heat-pretreated hearts compared to sham-treated controls (6.6 +/- 3.3. vs. 17.8 +/- 12.0 nmol/g wet wt). The findings suggest that mitigation of membrane phospholipid degradation is a potential mechanism of heat stress-mediated protection against the deleterious effects of ischemia and reperfusion on cardiac cells.
van der Vusse
G J
GJ
Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, The Netherlands.
Cornelussen
R N
RN
Roemen
T H
TH
Snoeckx
L H
LH
D000818:Animals; D016718:Arachidonic Acid / Q000032:analysis*; D003402:Creatine Kinase / Q000032:analysis; D003593:Cytoplasm / Q000201:enzymology; D005227:Fatty Acids / Q000032:analysis; D006358:Hot Temperature / Q000627:therapeutic use*; D008297:Male; D008563:Membrane Lipids / Q000032:analysis; D017202:Myocardial Ischemia / Q000517:prevention & control*; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D009206:Myocardium / Q000737:chemistry / Q000166:cytology / Q000201:enzymology; D010743:Phospholipids / Q000032:analysis; D051381:Rats; D011917:Rats, Inbred Lew; D013312:Stress, Physiological / Q000378:metabolism*
D005227:Fatty Acids; D008563:Membrane Lipids; D010743:Phospholipids; D016718:Arachidonic Acid; D003402:Creatine Kinase