Neuronal injury in experimental status epilepticus in the rat: role of hypoxia.
While it seems axiomatic that hypoxia is a risk factor for neuronal death during prolonged seizures, the classic neuropathologic literature does not confirm such an association. We investigated this issue by inducing status epilepticus in normoxic (PaO2 approximately 100 mmHg) and hypoxia (PaO2 approximately 50 mmHg) rats, using heat-shock protein (HSP) expression as an index of early cell injury and acid fuchsin staining to detect cell death. Neither stress protein induction nor neuronal death was increased in the selectively vulnerable CA3c region of hippocampus, or in cerebral cortex, of hypoxic compared to normoxic animals. These data support the concept that moderate hypoxia is not a risk factor for brain injury from status epilepticus.
Sasahira
M
M
Department of Neurology, University of Pittsburgh School of Medicine, PA 15213, USA.
Simon
R P
RP
Greenberg
D A
DA
D000818:Animals; D001640:Bicuculline; D001930:Brain Injuries / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D016923:Cell Death / Q000502:physiology; D006360:Heat-Shock Proteins / Q000032:analysis; D002534:Hypoxia, Brain / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D007150:Immunohistochemistry; D008297:Male; D009419:Nerve Tissue Proteins / Q000032:analysis; D009474:Neurons / Q000473:pathology* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012307:Risk Factors; D013226:Status Epilepticus / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology
D006360:Heat-Shock Proteins; D009419:Nerve Tissue Proteins; D001640:Bicuculline