title: [Effect of calcium antagonist nimodipine and induced hypertension on cerebral vessel reactivities, cerebral blood flow, cerebral edema and infarction in cats with one hour middle-cerebral-artery occlusion].
abstract: Treatment with the calcium entry blocker nimodipine is recommended as effective therapy for cerebral ischemia due to cerebral vasospasm or cerebral thrombosis. On the other hand, treatment with induced hypertension is a widely accepted measure to reverse ischemic deficits caused by vasospasm. Thus, a combination of the two regimens--nimodipine and induced hypertension--may have real benefits for cerebral ischemia. But it is possible that the benefit of one is abolished by adverse effects of the other, or that a combination of both may not be as effective as the use of only one therapy. In order to investigate these problems, the effects of nimodipine and induced hypertension on cerebral vessel, cerebral blood flow, cerebral edema and cerebral infarction using a one hour middle-cerebral-artery occlusion model in cats. Twenty-one anesthetized cats were divided into a control group, the nimodipine-treated group, and the nimodipine-and-induced-hypertension group. There were seven cats in each group. Occlusion of the middle cerebral artery (MCA) was continued for one hour in each animal. Induced hypertension was a little higher than resting values, and it was continued for only one hour during MCA occlusion, brought on by instillation of dopamine. Cerebral pial arteries dilated much more prominently during and after the occlusion of MCA in the nimodipine-and-induced-hypertension group than other groups. Although cerebral blood flow in the nimodipine group, and the nimodipine-and-induced-hypertension group increased more in the non-ischemic hemisphere, the most remarkable increase was seen around the infarcted cortex in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Neurosurgery, Nara Medical University.
authors.forename: T
authors.initials: T
authors.lastname: Sakaki
authors.forename: T
authors.initials: T
authors.lastname: Ishida
authors.forename: Y
authors.initials: Y
authors.lastname: Sasaoka
authors.forename: S
authors.initials: S
authors.lastname: Thunoda
authors.forename: S
authors.initials: S
authors.lastname: Utsumi
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D001929:Brain Edema / Q000473:pathology / Q000517:prevention & control*; D002545:Brain Ischemia / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D002415:Cats; D002536:Cerebral Arteries / Q000187:drug effects* / Q000503:physiopathology; D002544:Cerebral Infarction / Q000473:pathology / Q000517:prevention & control*; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D003250:Constriction; D004298:Dopamine / Q000627:therapeutic use; D009553:Nimodipine / Q000627:therapeutic use*; D014664:Vasodilation / Q000187:drug effects
chemical_list: D009553:Nimodipine; D004298:Dopamine