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Titolo:
DELAYED POSTISCHEMIC HYPERTHERMIA IN AWAKE RATS WORSENS THE HISTOPATHOLOGICAL OUTCOME OF TRANSIENT FOCAL CEREBRAL-ISCHEMIA
Autore:
KIM Y; BUSTO R; DIETRICH WD; KRAYDIEH S; GINSBERG MD;
Indirizzi:
UNIV MIAMI,SCH MED,DEPT NEUROL D45,CEREBRAL VASC DIS RES CTR,POB 016960 MIAMI FL 33101 UNIV MIAMI,SCH MED,DEPT NEUROL D45,CEREBRAL VASC DIS RES CTR MIAMI FL33101
Titolo Testata:
Stroke
fascicolo: 12, volume: 27, anno: 1996,
pagine: 2274 - 2280
SICI:
0039-2499(1996)27:12<2274:DPHIAR>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
BRAIN ENERGY-METABOLISM; ARTERY OCCLUSION; FOREBRAIN ISCHEMIA; NEURONAL DAMAGE; MILD HYPERTHERMIA; ACUTE STROKE; BLOOD-FLOW; INFARCT VOLUME; HYPOTHERMIA; TEMPERATURE;
Keywords:
CEREBRAL ISCHEMIA, FOCAL; HYPERTHERMIA; MIDDLE CEREBRAL ARTERY OCCLUSION; NEURONAL DAMAGE; RATS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
64
Recensione:
Indirizzi per estratti:
Citazione:
Y. Kim et al., "DELAYED POSTISCHEMIC HYPERTHERMIA IN AWAKE RATS WORSENS THE HISTOPATHOLOGICAL OUTCOME OF TRANSIENT FOCAL CEREBRAL-ISCHEMIA", Stroke, 27(12), 1996, pp. 2274-2280

Abstract

Background and Purpose Over the past several years, it has been demonstrated that mild intraischemic or immediate postischemic hyperthermiaworsens ischemic outcome in models of global and focal ischemia. Periods of hyperthermia are commonly seen in patients after stroke and cardiac arrest. The hypothesis tested in this study was that a brief hyperthermic period, even when occurring days after an ischemic insult, has detrimental effects on the pathological outcome of focal ischemia. Methods Rats were subjected to 60 minutes of transient middle cerebral artery occlusion by insertion of an intraluminal filament. Twenty-fourhours after reperfusion, awake rats were subjected to temperature modulation for 3 hours in a heating chamber. The brain temperature was equilibrated to either 37 degrees C to 38 degrees C, 39 degrees C, or 40degrees C. Changes in rectal temperature and blood glucose concentration were evaluated during and just after temperature modulation. Behavioral tests were also assessed. Three days after temperature modulation, brains were perfusion-fixed, and infarct volumes were determined. Results In animals with 40 degrees C hyperthermia, cortical and total infarct volumes were markedly greater (92.2+/-63.1 and 126.5+/-72.3 mm(3) [mean+/-SD], respectively) than in normothermic rats (14.4+/-12.7 and 42.4+/-19.2 mm(3)) and in animals with 39 degrees C hyperthermia (16.5+/-28.7 and 40.9+/-34.3 mm(3)) (P<.05), whereas there was no significant difference between normothermic and 39 degrees C hyperthermic animals. In addition, animals with 40 degrees C hyperthermia displayed worsened neurological scores compared with normothermic and 39 degrees C hyperthermic rats. In the 39 degrees C hyperthermia group, rectal temperatures were significantly lower (by 0.2 degrees C to 0.5 degrees C) than brain temperatures throughout the modulation period. Conclusions The present findings provide evidence that, after a transient focal ischemic insult, the postischemic brain becomes abnormally sensitive to the effects of delayed temperature elevation, even of moderate degree. The threshold for aggravation of ischemic injury by delayed hyperthermia appears to be approximately 40 degrees C. Body-temperature measurements, in both awake and anesthetized animals, may not accurately reflect brain temperature under these conditions. The present study stresses that fever of even moderate degree in the days following brain ischemia may markedly exacerbate brain injury.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/01/20 alle ore 17:39:31