Hyperthermia delayed by 24 hours aggravates neuronal damage in rat hippocampus following global ischemia

R. C. Baena, R. Busto, W. Dalton Dietrich, M. Y.T. Globus, Myron D. Ginsberg

Research output: Contribution to journalArticlepeer-review

137 Scopus citations


We investigated whether moderate, transient whole-body hyperthermia (≡39.6 °C), if imposed 1 day following a brief episode of forebrain ischemia, would affect the neuropathologic outcome. Forty-two Wistar rats were subjected to either a 5- or 7-minute period of bilateral common carotid artery occlusion plus hypotension (50 mm Hg), or to the equivalent sham procedure. Twenty-four hours later, rats of one subgroup were placed into a hyperthermic chamber containing high-intensity lamps designed to elevate rectal temperature to 39 to 40 °C for 3 hours. Normothermic sub-groups received the same procedures, but the heating lamps were turned off. Eight days after brain ischemia or the sham procedure, brains were perfusion- fixed, and numbers of ischemic-appearing CA1 pyramidal neurons were counted. In rats with 7-minute forebrain ischemia, delayed hyperthermia increased mean numbers of ischemic neurons by 2.6- to 2.7-fold in all subsectors of area CA1 (p < 0.05, ANOVA). Delayed hyperthermia in 5-minute ischemic rats also tended to increase mean numbers of ischemic neurons (by 11-fold in lateral, 6-fold in middle, and 5-fold in medial CA1 subsectors), but these differences were not statistically significant. We conclude that moderate, transient hyperthermia, even if occurring 1 day after a 7-minute global ischemic insult, exacerbates the extent of ischemic neuronal injury.

Original languageEnglish (US)
Pages (from-to)768-773
Number of pages6
Issue number3
StatePublished - Mar 1997

ASJC Scopus subject areas

  • Clinical Neurology


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