Faculty Collaboration Database

Cardioprotection is strain dependent in rat in response to whole body hyperthermia. Am J Physiol Heart Circ Physiol 2001 Mar;280(3):H1208-14

Date

02/17/2001

Pubmed ID

11179065

DOI

10.1152/ajpheart.2001.280.3.H1208

Scopus ID

2-s2.0-0034967040 (requires institutional sign-in at Scopus site)   15 Citations

Abstract

Previous results showed a genetic component to cardioprotection. Therefore, we investigated the heat shock response in Wistar and Sprague-Dawley (SD) rats at 24 and 48 h. Rats were subjected to whole body hyperthermia achieving colonic temperatures of 40 or 42 degrees C for 20 min. After recovery hearts were excised for protein measurements or were subjected to 30 min of ischemia and then 2 h of reperfusion. Heat shock protein (HSP) expression was determined by Western blotting and infarct size was determined by triphenyltetrazolium staining. All groups of SD and Wistar rats demonstrated HSP72 and HSP90 induction at both time points in response to a heat stress of 42 degrees C. At 24 h there was only a significant reduction in infarct size seen in control vs. small SD (60.0 +/- 4.8 vs. 26.5 +/- 2.3) rats. However, at 48 h control versus small SD (60.0 +/- 4.8 vs. 17.6 +/- 3.8) and Wistar (59.4 +/- 4.3 vs. 29.8 +/- 6.0) and control versus large SD (53.7 +/- 2.6 vs. 19.8 +/- 4.7) and Wistar (57.3 +/- 1.6 vs. 34.5 +/- 2.8) rats demonstrated a significant reduction in infarct size with a greater reduction observed in SD rats. We conclude that heat shock-induced cardioprotection in rats is dependent on strain, temperature, time after stress, and size.

Author List

Patel HH, Hsu A, Gross GJ

MESH terms used to index this publication - Major topics in bold

Animals
Blood Pressure
Fever
Gene Expression
Genetic Predisposition to Disease
HSP70 Heat-Shock Proteins
HSP90 Heat-Shock Proteins
Heart Rate
Heat-Shock Response
Male
Myocardial Infarction
Myocardial Reperfusion Injury
Rats
Rats, Sprague-Dawley
Rats, Wistar
Species Specificity