Postischemic Spontaneous Hyperthermia and Its Effects in Middle Cerebral Artery Occlusion in the Rat

• Published in: Experimental neurology Vol. 163; no. 2; pp. 399 - 407
• Main Authors: Reglodi, Dora, Somogyvari-Vigh, Aniko, Maderdrut, Jerome L., Vigh, Sandor, Arimura, Akira
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Inc 01.06.2000; Elsevier
• Subjects: Animals; Biological and medical sciences; Brain Ischemia - etiology; Brain Ischemia - pathology; Cerebral Infarction - etiology; Cerebral Infarction - pathology; cerebral ischemia; Fever - complications; Fever - pathology; focal ischemia; hyperthermia; Infarction, Middle Cerebral Artery - complications; Infarction, Middle Cerebral Artery - pathology; Male; Medical sciences; middle cerebral artery occlusion; Neurology; Rats; stroke; Vascular diseases and vascular malformations of the nervous system; focal ischemia; hyperthermia; stroke; cerebral ischemia; middle cerebral artery occlusion; Nervous system diseases; Stroke; Pathophysiology; Rat; Spontaneous; Rodentia; Middle cerebral artery; Cardiovascular disease; Transitory; Cerebral disorder; Vascular disease; Vertebrata; Mammalia; Ischemia; Animal; Central nervous system disease; Hyperthermia; Cerebrovascular disease; Brain (vertebrata)
• ISSN: 0014-4886; 1090-2430
• DOI: 10.1006/exnr.2000.7367

This study examined the time course and effects of postischemic spontaneous hyperthermia after transient and permanent focal ischemia. Rats underwent a 90-min, 120-min, or permanent middle cerebral artery occlusion (MCAO). Body temperatures started rising 15–20 min after MCAO and reached 39–40.5°C during the first hour. Sustained hyperthermia was observed during the rest of the first 24 h. In another experiment, rats were subjected to the same interventions, but a normothermic body temperature was maintained. Spontaneous hyperthermia significantly increased the infarct volumes measured 48 h after MCAO in all groups. Reperfusion 2 h after the onset of ischemia was not beneficial in the hyperthermic animals in contrast to the normothermic group. We also examined the effect of spontaneous hyperthermia on the temporal progression of infarcted and penumbral areas 4, 12, or 48 h after MCAO. During spontaneous hyperthermia, penumbral areas became infarcted areas more rapidly, which was most expressed at 4 h. These findings demonstrate that severe spontaneous hyperthermia can occur in rats after MCAO and that it not only increases the infarct volumes in both transient and permanent ischemia, but also accelerates the incorporation of penumbral areas into necrotic areas, which significantly decreases the window of opportunity for therapeutic interventions.