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Heat shock improves ischemic tolerance of hypertrophied rat hearts.

作者信息

Cornelussen R, Spiering W, Webers J H, De Bruin L G, Reneman R S, van der Vusse G J, Snoeckx L H

机构信息

Department of Physiology, University of Limburg, Maastricht, The Netherlands.

出版信息

Am J Physiol. 1994 Nov;267(5 Pt 2):H1941-7. doi: 10.1152/ajpheart.1994.267.5.H1941.

DOI:10.1152/ajpheart.1994.267.5.H1941
PMID:7977825
Abstract

The postischemic recovery of hypertrophied hearts was studied 24 h after total body hyperthermia. To this end, anesthetized aortic-banded and sham-operated rats were subjected to heat shock (AoBHS and ShamHS, respectively). Cardiac hypertrophy was induced 8 wk earlier. In isolated ejecting hearts, functional recovery after 45 min of global ischemia was poor and moderate in nonheated (control) hypertrophied (AoBC) and nonheated (control) nonhypertrophied (ShamC) hearts, respectively. Heat shock significantly improved postischemic recovery in both AoBHS and ShamHS hearts. This improvement of functional recovery was associated with a significant reduction of the duration of arrhythmias. In addition, coronary flow was significantly higher in both types of heat-shocked hearts than in the corresponding control hearts during the preischemic as well as the postischemic period. Postischemic endocardial flow, assessed using radioactive microspheres, was significantly improved in AoBHS hearts. Compared with the corresponding control hearts, the native endogenous catalase activity was not changed in AoBHS hearts but was significantly increased in ShamHS hearts. The present findings suggest that the postischemic functional improvement after total body hyperthermia can be explained by increased and more homogeneous myocardial perfusion, which may also reduce the duration of postischemic arrhythmias. This effect is especially beneficial for the hypertrophied heart, which is known to be extremely vulnerable to the ischemic insult probably caused by subendocardial underperfusion.

摘要

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引用本文的文献

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Heat shock protein 70 acts as a potential biomarker for early diagnosis of heart failure.热休克蛋白 70 可作为心力衰竭早期诊断的潜在生物标志物。
PLoS One. 2013 Jul 9;8(7):e67964. doi: 10.1371/journal.pone.0067964. Print 2013.
2
Heat stress contributes to the enhancement of cardiac mitochondrial complex activity.热应激有助于增强心脏线粒体复合物的活性。
Am J Pathol. 2001 May;158(5):1821-31. doi: 10.1016/S0002-9440(10)64138-7.
3
Heat stress pretreatment mitigates postischemic arachidonic acid accumulation in rat heart.热应激预处理减轻大鼠心脏缺血后花生四烯酸的蓄积。
Mol Cell Biochem. 1998 Aug;185(1-2):205-11. doi: 10.1023/a:1016574720342.