This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Inoue, T. Articles by Kogure, K. Search for Related Content PubMed PubMed Citation Articles by Inoue, T. Articles by Kogure, K.

Stroke, Vol 23, 739-745, Copyright © 1992 by American Heart Association

ARTICLES

Emphasized selective vulnerability after repeated nonlethal cerebral ischemic insults in rats

T Inoue, H Kato, T Araki and K Kogure
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.

BACKGROUND AND PURPOSE: We examined the density and distribution of brain damage after repeated periods of nonlethal ischemic insult in rats in comparison with damage after single lethal periods of ischemic insult. METHODS: Transient cerebral ischemia was induced by four-vessel occlusion for 3, 10, 20, and 30 minutes, and 3-minute periods of ischemia were repeated two, three, or five times at 1-hour intervals, followed by 7 days of survival. RESULTS: Three minutes of ischemia produced no brain damage, but 10-30 minutes of ischemia produced neuronal damage, depending on the length of ischemia, to the selectively vulnerable forebrain regions such as hippocampal CA1 and CA4 subfields, neocortex, striatum, and ventral thalamus, as well as to the brain stem structures (medial geniculate body, substantia nigra, and inferior colliculus) and cerebellar Purkinje cells. Two 3-minute periods of ischemic insult produced neuronal damage to the hippocampal CA1 subfield. Three and five 3-minute insults produced neuronal damage extensively to the selectively vulnerable forebrain areas. An intense cumulative effect of damage was observed in the ventral thalamus, whereas the substantia nigra and the inferior colliculus were resistant to repeated ischemic insults. CONCLUSIONS: Our data indicate that the density and distribution of neuronal damage after repeated ischemic insults are altered as compared with after single ischemia.

This article has been cited by other articles:

				K.-H. Ladwig, A. Schoefinius, G. Dammann, R. Danner, R. Gürtler, and R. Herrmann Long-Acting Psychotraumatic Properties of a Cardiac Arrest Experience Am J Psychiatry, June 1, 1999; 156(6): 912 - 919. [Abstract] [Full Text]