van der Vusse G J, Cornelussen R N, Roemen T H, Snoeckx L H
Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, The Netherlands.
Mol Cell Biochem. 1998 Aug;185(1-2):205-11. doi: 10.1023/a:1016574720342.
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.
已知对心脏进行热应激预处理可在24小时后保护该器官免受缺血/再灌注损伤。膜磷脂降解导致多不饱和脂肪酸（如花生四烯酸）在组织中积累，这被认为在缺血/再灌注诱导损伤的多因素过程中起重要作用。本研究旨在检验以下假设：热应激可减轻心肌组织中花生四烯酸的缺血后积累，这是膜磷脂降解增强的一个标志。实验在全身热处理（42℃，15分钟）24小时后的大鼠离体心脏或假处理（对照组）24小时后的大鼠离体心脏上进行。心脏缺血45分钟，再灌注45分钟。热预处理显著改善了离体大鼠心脏缺血后的血流动力学性能。肌酸激酶的释放从30±14（对照组）降至17±5单位/克湿重每45分钟（热预处理组）（p≤0.05）。此外，发现诱导型热应激蛋白HSP70的组织含量在热处理后24小时增加了3倍。热预处理心脏和对照心脏缺血前组织中的花生四烯酸水平没有差异。与假处理对照组相比，热预处理心脏缺血后心室中的花生四烯酸含量显著降低（6.6±3.3对17.8±12.0纳摩尔/克湿重）。这些发现表明，减轻膜磷脂降解是热应激介导的保护心脏细胞免受缺血和再灌注有害影响的潜在机制。
