Protective effects of Ca++-antagonist agents on the cerebral electrical activity during anoxia in the rat.
Transient anoxia obtained in curarized rats by momentary stopping of the artificial respiration (80 sec duration) induced a failure of the cerebral electrical activity. This effect was characterized by cessation of the spontaneous unitary discharge of cortical neurons and reduction of amplitude of somatosensory evoked potentials. Pretreatment with flunarizine (10 mg/kg/os) or suloctidil (50 mg/kg/os) induced a distinct improvement of the resistance to anoxia and of the recovery of the cerebral electrical activity.
D000818:Animals; D001921:Brain / Q000187:drug effects*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002936:Cinnarizine / Q000031:analogs & derivatives / Q000494:pharmacology; D004594:Electrophysiology; D005071:Evoked Potentials / Q000187:drug effects; D005444:Flunarizine; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D009474:Neurons / Q000502:physiology; D051381:Rats; D013468:Suloctidil / Q000494:pharmacology
D002121:Calcium Channel Blockers; D002936:Cinnarizine; D005444:Flunarizine; D013468:Suloctidil