title: Vulnerability to cerebral hypoxic-ischemic insult in neonatal but not in adult rats is in parallel with disruption of the blood-brain barrier.
abstract: OBJECTIVE
  Vulnerability to cerebral hypoxic-ischemic (H-I) insult and its relation to disruption of the blood-brain barrier were investigated in postnatal rats.
  
  
  METHODS
  Pups of postnatal day (P) 7, P14, and P21 underwent ligation of a unilateral carotid artery and were exposed to hypoxic conditions. For the detection of early-phase deterioration, brains were perfusion-fixed 24 hours after H-I insult and examined by argyrophil III method. For the detection of later infarction, animals were fixed at 72 hours after the H-I insult.
  
  
  RESULTS
  In either case, tissue damage was detected in the striatum, parietal cortex, and hippocampus. The vulnerability of P7 and P21 rats was remarkable, as compared with P14 rats. Although the developmental status of the vasculature was not significantly different at each age, the permeability of IgG after H-I injury was prominent in P7 rats and to a lesser extent in P14 rats. In P21 rats, however, there was little IgG leakage even 24 hours after the insult. Dexamethasone pretreatment blocked the extravasation of IgG and reduced the damaged tissue in P7 and P14 rats but not in P21 rats. Percentages of reduction in infarcted areas by the dexamethasone became smaller in proportion to ages.
  
  
  CONCLUSIONS
  The results suggest that in younger rats vulnerability to H-I insult was in parallel with permeability of the blood-brain barrier, whereas in adults in might be more dependent on cellular vulnerability.
authors.affiliation: Department of Pediatrics, Nagoya City University Medical School, Japan. muramatu@med.nagoya-cu.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Muramatsu
authors.forename: A
authors.initials: A
authors.lastname: Fukuda
authors.forename: H
authors.initials: H
authors.lastname: Togari
authors.forename: Y
authors.initials: Y
authors.lastname: Wada
authors.forename: H
authors.initials: H
authors.lastname: Nishino
mesh_terms: D000375:Aging / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn / Q000254:growth & development / Q000502:physiology*; D001808:Blood Vessels / Q000254:growth & development / Q000378:metabolism; D001812:Blood-Brain Barrier / Q000502:physiology*; D001921:Brain / Q000098:blood supply / Q000473:pathology*; D001927:Brain Diseases / Q000473:pathology* / Q000503:physiopathology; D002545:Brain Ischemia / Q000473:pathology* / Q000503:physiopathology; D002199:Capillary Permeability / Q000502:physiology; D003907:Dexamethasone / Q000494:pharmacology; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology; D000860:Hypoxia / Q000473:pathology* / Q000503:physiopathology; D007074:Immunoglobulin G / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D005938:Glucocorticoids; D007074:Immunoglobulin G; D003907:Dexamethasone