Spontaneous cerebral hypothermia diminishes focal infarction in rat brain

• Published in: Stroke (1970) Vol. 23; no. 12; pp. 1812 - 1816
• Main Authors: MOYER, D. J, WELSH, F. A, ZAGER, E. L, GARCIA, J. H
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 01.12.1992
• Subjects: Animals; Biological and medical sciences; Body Temperature; Brain - physiopathology; Cerebral Infarction - pathology; Cerebral Infarction - physiopathology; Cerebral Infarction - therapy; Diseases of the nervous system; Hypothermia, Induced; Male; Medical sciences; Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects); Rats; Rats, Wistar; Nervous system diseases; Rat; Rodentia; Central nervous system; Cardiovascular disease; Vascular disease; Vertebrata; Mammalia; Treatment; Ischemia; Animal; Brain (invertebrata); Technique; Hypothermia
• ISSN: 0039-2499; 1524-4628
• DOI: 10.1161/01.STR.23.12.1812

Brain temperature during ischemia is known to strongly influence the extent of cellular injury. The objectives of the present study were to determine the effect of severe focal ischemia on brain temperature and to assess the influence of those changes on focal infarction. Severe focal ischemia was produced in rats using permanent occlusion of the distal middle cerebral artery combined with transient (60-minute) bilateral carotid artery occlusion. The temperature of the ischemic focus was measured with a small subdural probe. Three groups of rats were studied. In the first group, brain temperature was permitted to decline spontaneously to 32 degrees C after occlusion. In the second, brain temperature was maintained at 37.5 degrees C during occlusion. In the third group, the brain temperature was maintained at 37.5 degrees C for 40 minutes postocclusion before cooling. After recovery for 24 hours, the volume of infarction was measured in histological sections. In the absence of cranial heating, the brain temperature fell to 33 degrees C by 10 minutes postocclusion, and infarct volume was 19 +/- 9 mm3 (mean +/- SEM; n = 6). Maintaining brain temperature at 37.5 degrees C increased the volume of infarction to 82 +/- 16 mm3 (n = 7; p < 0.001). Delayed cooling did not prevent the increase in infarct volume (75 +/- 16 mm3; n = 6). These results demonstrate that in the present model of transient focal ischemia, spontaneous cooling of the brain during ischemia diminishes the extent of focal infarction, relative to that observed when cerebral hypothermia is prevented or delayed for 40 minutes.