Dissociation of Heat Shock Proteins Expression with Ischemic Tolerance by Whole Body Hyperthermia in Rat Heart

• Published in: Journal of molecular and cellular cardiology Vol. 30; no. 6; pp. 1163 - 1172
• Main Authors: Qian, Yong-Zhen, Shipley, Joshua B., Levasseur, Joseph E., Kukreja, Rakesh C.
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.06.1998
• Subjects: Animals; Heat shock proteins; Heat-Shock Proteins - metabolism; Heat-Shock Response; Hemodynamics; Hyperthermia; Hyperthermia, Induced - adverse effects; Infarction; Ischemia; Male; Myocardial Infarction - metabolism; Myocardial Infarction - pathology; Myocardial Ischemia - metabolism; Myocardial Reperfusion; Myocardium - metabolism; Myocardium - pathology; Rats; Rats, Sprague-Dawley; Time Factors; Heat shock proteins; Infarction; Ischemia; Hyperthermia
• ISSN: 0022-2828; 1095-8584
• DOI: 10.1006/jmcc.1998.0680

Heat shock (HS) results in the expression of heat shock proteins (hsp) and confers tolerance against subsequent ischemic injury. We examined the extent of myocardial protectionin vivo, and determined the level of hsp expression induced by HS as a function of time. Anesthetized rats were subjected to HS by raising core temperature to 42°C for 15 min and they were then allowed to recover from 2 to 30 h (n=8–11 for each time point). At the appropriate time, animals were subjected to 30 min of ischemia via ligation of the LAD, followed by 90 min of reperfusion. Infarct size was determined by tetrazolium staining and hsp expression was assessed by Western blots. Following ischemia/reperfusion, the infarct sizes (% risk area) were 51.3±3.7, 41.0±7.7, 48.0±6.9 after 2, 4 and 12 h of HS, which were not significantly different from 39.2±2.75 in non heat-shocked animals (P>0.05). In contrast, the infarct size was reduced significantly to 11.0±3.1% in 24 h HS group (P<0.01vnon-heat-shocked control, 2, 4 and 12 h HS groups), but increased back to 40.0±3.2% (P<0.01) by 30 h after HS. No major significant differences in the mean arterial blood pressure, heart rate or rate pressure product was observed between different groups. The synthesis of 72- and 27-kD hsp in HS groups was rapid, reaching >80% of maximum within 4 h of initial insult and peaked by 12 h, whereas the protective effect of HS was absent at these time points. We conclude that ischemic tolerance afforded by HS cannot be solely explained on the basis of hsp expression, and may be dependent on factors such as post-translational modifications, translocation of hsps or some other as yet unidentified factors.