Brief hypoxia-ischemia initially damages cerebral neurons.
Rats were studied during cerebral hypoxic ischemia to determine whether neurons or blood vessels suffered the first damage. Ten or more minutes of unilateral carotid artery occlusion combined with systemic hypoxemia (PaO-2, 21 mm Hg) produced neuronal but not vascular damage in the ipsilateral cerebral hemispheres of 18 of 29 rats (62%); two and five minute stresses caused no visible neuronal abnormalities. The longer exposures produced more widespread damage, and neuronal loss and gliomesodermal reaction were evident after prolonged survival. Early neuronal changes correlated with abnormalities of motor behavior (P less than .005). Despite neuronal damage that was sometimes extensive, vascular no-reflow developed in only one of 24 animals after 20 and 30 minutes of hypoxia-ischemia. Production of neuronal and neurological abnormalities in the absence of hypotension or vascular no-reflow indicates that hypoxia-ischemia initially damaged cerebral neurons.
D000769:Anesthesia, Inhalation; D000818:Animals; D001921:Brain / Q000473:pathology*; D002244:Carbon; D002339:Carotid Arteries; D002560:Cerebrovascular Circulation; D004987:Ethers; D000860:Hypoxia / Q000139:chemically induced; D002534:Hypoxia, Brain / Q000473:pathology*; D007275:Injections, Intravenous; D002546:Ischemic Attack, Transient / Q000473:pathology* / Q000503:physiopathology; D008026:Ligation; D008297:Male; D009043:Motor Activity; D009474:Neurons / Q000473:pathology*; D009589:Nitrogen Oxides / Q000008:administration & dosage; D051381:Rats; D013997:Time Factors
D004987:Ethers; D009589:Nitrogen Oxides; D002244:Carbon