Hypothermia reduces 72-kDa heat-shock protein induction in rat brain after transient forebrain ischemia.
OBJECTIVE
We examined the influence of concurrent moderate hypothermia (30 degrees C) and transient forebrain ischemia on the induction of 72-kDa heat-shock protein and neuronal damage in male Wistar rats.


METHODS
Experimental groups included: normothermic with 8 minutes of transient forebrain ischemia (group 1, n = 7), hypothermic without ischemia (group 2, n = 9), and hypothermic (30 degrees C) with 8 minutes of transient forebrain ischemia (group 3, n = 5). Intense 72-kDa heat-shock protein immunoreactivity was demonstrated in rat forebrain 48 hours after induction of normothermic forebrain ischemia (group 1); it was not detected in the brain of animals subjected to hypothermia without ischemia (group 2), and hypothermia during ischemia (group 3) significantly inhibited its expression compared with that in normothermic ischemia animals (group 1).


CONCLUSIONS
These observations suggest that 72-kDa heat-shock protein induction is not the mechanism by which moderate hypothermia protects against ischemic cell damage.
Chopp
M
M
Department of Neurology, Henry Ford Hospital, MI 48202.
Li
Y
Y
Dereski
M O
MO
Levine
S R
SR
Yoshida
Y
Y
Garcia
J H
JH
D000818:Animals; D006360:Heat-Shock Proteins / Q000378:metabolism*; D007036:Hypothermia, Induced; D002546:Ischemic Attack, Transient / Q000378:metabolism* / Q000628:therapy; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D006360:Heat-Shock Proteins