Prenatal ischemia reduces neuronal injury caused by neonatal hypoxia-ischemia in rats.
To determine whether 'ischemic tolerance', first described in adult rodents, exists in fetal and neonatal rats, a comparison of brain injury was made between two groups of rat pups following neonatal hypoxia-ischemia (HI). One group of rat pups had previously been subjected to HI in utero (HI + HI); the other had been subjected to a sham operation (SH + HI). Brain infarct size and neuronal injury were measured 24 h after the neonatal HI insult. As indicated by 2,3,5-triphenyltetrazolium chloride staining and pathological examination, cerebral damage was significantly less in the HI+ HI group than in the SH + HI group. Induction of heat shock protein 70 (hsp70) was immunohistochemically detectable in both groups 24 h after the neonatal HI, and was proportional to the extent of tissue damage. The ischemic tolerance phenomenon observed in immature rats does not appear to be a result of induction of hsp70.
Cai
Z
Z
Department of Pediatrics/Newborn Medicine, University of Mississippi Medical Center, Jackson 39216, USA.
Fratkin
J D
JD
Rhodes
P G
PG
D000818:Animals; D000831:Animals, Newborn; D015153:Blotting, Western; D002545:Brain Ischemia / Q000473:pathology*; D002544:Cerebral Infarction / Q000473:pathology*; D018840:HSP70 Heat-Shock Proteins / Q000096:biosynthesis; D002534:Hypoxia, Brain / Q000473:pathology*; D007150:Immunohistochemistry; D009474:Neurons / Q000473:pathology*; D051381:Rats
D018840:HSP70 Heat-Shock Proteins