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Temporal profile of neuronal damage in a model of transient forebrain ischemia

Pulsinelli, William A., Brierley, James B., Plum, Fred·1982·Annals of Neurology

Abstract

This study examined the temporal profile of ischemic neuronal damage following transient bilateral forebrain ischemia in the rat model of four‐vessel occlusion. Wistar rats were subjected to transient but severe forebrain ischemia by permanently occluding the vertebral arteries and 24 hours later temporarily occluding the common carotid arteries for 10, 20, or 30 minutes. Carotid artery blood flow was restored and the rats were killed by perfusion‐fixation after 3, 6, 24, and 72 hours. Rats with postischemic convulsions were discarded. Ischemic neuronal damage was graded in accordance with conventional neuropathological criteria. Ten minutes of four‐vessel occlusion produced scattered ischemic cell change in the cerebral hemispheres of most rats. The time to onset of visible neuronal damage varied among brain regions and in some regions progressively worsened with time. After 30 minutes of ischemia, small to medium‐sized striatal neurons were damaged early while the initiation of visible damage to hippocampal neurons in the h1 zone was delayed for 3 to 6 hours. The number of damaged neurons in neocortex (layer 3, layers 5 and 6, or both) and hippocampus (h1, h3–5, paramedian zone) increased significantly (p < 0.01) between 24 and 72 hours. The unique delay in onset of ischemic cell change and the protracte increase in its incidence between 24 and 72 hours could reflect either delayed‐appearance of ischemic change in previously killed neurons or a delayed insult that continued to jeopardize compromised but otherwise viable neurons during the postischemic period.

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Metadata

Authors
Pulsinelli, W. A., Brierley, J. B., & Plum, F.
Venue
Annals of Neurology
Publisher
Wiley
Published
1982-05
Volume
11
Issue
5
Pages
491-498
ISSN
  • 0364-5134 (ISSN-L)
  • 1531-8249
OpenAlex
W1982892406
Cited by
2,675
References
0
FWCI
28.04
Type
journal article
Language
en
Open access
closed

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