Heat stress increases cardiac HSP72i but fails to reduce myocardial infarct size in rabbits 24 hours later.
Recent reports suggest that delayed myocardial protection ("second window of preconditioning") occurs 24 hours after brief ischemic or thermal stress. In order to test this hypothesis, we subjected New Zealand White rabbits to a heating regimen (42 degrees C for 15-20 minutes). Twenty four hours later, the effect of heat stress on infarct size was determined by conducting a 30 minute ischemia/3 hour reperfusion protocol. In a separate group of rabbits, Western blot analysis was used to verify that the heating regimen increased expression of HSP72i. The size of the region at risk was delineated by infusion of Unisperse blue and infarcted myocardium was identified by incubation of left ventricular slices in triphenyl tetrazolium chloride. In contrast to expectations, induction of HSP72i with thermal stress was not effective in limiting infarct size in rabbits 24 hours later, calling into question the concept that heat stress induces delayed or "second window" myocardial protection.
Saganek
L J
LJ
Vascular and Cardiac Diseases Section, Parke-Davis Pharmaceutical, Ann Arbor, Michigan 48105, USA. saganel@aa.wl.com
Ignasiak
D P
DP
Batley
B L
BL
Potoczak
R E
RE
Dodd
G
G
Gallagher
K P
KP
D000818:Animals; D015153:Blotting, Western; D050884:HSP72 Heat-Shock Proteins; D018882:Heat Stress Disorders / Q000378:metabolism* / Q000473:pathology; D006360:Heat-Shock Proteins / Q000096:biosynthesis*; D006358:Hot Temperature / Q000009:adverse effects; D019157:Ischemic Preconditioning, Myocardial; D009203:Myocardial Infarction / Q000378:metabolism* / Q000473:pathology; D011817:Rabbits; D013997:Time Factors
D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins