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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Hyperthermia induced after recirculation triggers chronic neurodegeneration in the penumbra zone of focal ischemia in the rat brain

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Author(s):
Favero-Filho, L. A. [1, 2] ; Borges, A. A. [1, 3] ; Grassl, C. [1, 3] ; Lopes, A. C. [1, 3] ; Sinigaglia-Coimbra, R. [1, 4, 5] ; Coimbra, C. G. [1, 3, 2]
Total Authors: 6
Affiliation:
[1] Univ Fed Sao Paulo, Lab Fisiopatol Clin & Expt, Escola Paulista Med, BR-04039032 Sao Paulo - Brazil
[2] Univ Fed Sao Paulo, Dept Neurol & Neurocirurgia, Escola Paulista Med, BR-04039032 Sao Paulo - Brazil
[3] Univ Fed Sao Paulo, Dept Med, Escola Paulista Med, BR-04039032 Sao Paulo - Brazil
[4] Univ Fed Sao Paulo, Ctr Microscopia Eletron, Escola Paulista Med, BR-04039032 Sao Paulo - Brazil
[5] Univ Fed Sao Paulo, COLSAN, Escola Paulista Med, BR-04039032 Sao Paulo - Brazil
Total Affiliations: 5
Document type: Journal article
Source: Brazilian Journal of Medical and Biological Research; v. 41, n. 11, p. 1029-1036, NOV 2008.
Web of Science Citations: 4
Abstract

Chronic neurodegenerative processes have been identified in the rat forebrain after prolonged survival following hyperthermia (HT) initiated a few hours after transient global ischemia. Since transient global ischemia and ischemic penumbra share pathophysiological similarities, this study addressed the effects of HT induced after recirculation of focal brain ischemia on infarct size during long survival times. Adult male Wistar rats underwent intra-luminal occlusion of the left middle cerebral artery for 60 min followed by HT (39.0-39.5°C) or normothermia. Control procedures included none and sham surgery with and without HT, and middle cerebral artery occlusion alone. Part I: 6-h HT induced at recirculation. Part II: 2-h HT induced at 2-, 6-, or 24-h recirculation. Part III: 2-h HT initiated at recirculation or 6-h HT initiated at 2-, 6- or 24-h recirculation. Survival periods were 7 days, 2 or 6 months. The effects of post-ischemic HT on cortex and striatum were evaluated histopathologically by measuring the area of remaining tissue in the infarcted hemisphere at -0.30 mm from bregma. Six-hour HT initiated from 6-h recirculation caused a significant decrease in the remaining cortical tissue between 7-day (N = 8) and 2-month (N = 8) survivals (98.46 ± 1.14 to 73.62 ± 8.99%, respectively). When induced from 24-h recirculation, 6-h HT caused a significant reduction of the remaining cortical tissue between 2- (N = 8) and 6-month (N = 9) survivals (94.97 ± 5.02 vs 63.26 ± 11.97%, respectively). These data indicate that post-ischemic HT triggers chronic neurodegenerative processes in ischemic penumbra, suggesting that similar fever-triggered effects may annul the benefit of early recirculation in stroke patients over the long-term. (AU)