We studied the possible role of prior ischemic stress as a protective
mechanism against cerebral infarction in rats. Two brief periods of gl
obal cerebral ischemia, separated by 24 h, did not cause cell death in
brain, but did produce neuronal stress, as demonstrated by induction
of the nonconstitutive 72 kDa heal shock protein (HSP72). Forty-eight
hours later, animals subjected to prior ischemia had smaller infarct f
rom permanent middle cerebral artery occlusion than did sham-operated
controls. These findings support an association between ischemia-induc
ed stress, HSP72 induction, and attenuation of injury from subsequent
focal cerebral ischemia.