Postischemic hypothermia. A critical appraisal with implications for clinical treatment.
The use of hypothermia to mitigate cerebral ischemic injury is not new. From early studies, it has been clear that cooling is remarkably neuroprotective when applied during global or focal ischemia. In contrast, the value of postischemic cooling is typically viewed with skepticism because of early clinical difficulties and conflicting animal data. However, more recent rodent experiments have shown that a protracted reduction in temperature of only a few degrees Celsius can provide sustained behavioral and histological neuroprotection. Conversely, brief or very mild hypothermia may only delay neuronal damage. Accordingly, protracted hypothermia of 32-34 degrees C may be beneficial following acute clinical stroke. A thorough mechanistic understanding of postischemic hypothermia would lead to a more selective and effective therapy. Unfortunately, few studies have investigated the mechanisms by which postischemic cooling conveys its beneficial effect. The purpose of this article is to evaluate critically the effects of postischemic temperature changes with a comparison to some current drug therapies. This article will stimulate new research into the mechanisms of lengthy postischemic hypothermia and its potential as a therapy for stroke patients.
Colbourne
F
F
Department of Clinical Neurosciences, Faculty of Medicine, University of Calgary, Alberta, Canada.
Sutherland
G
G
Corbett
D
D
D000818:Animals; D001921:Brain / Q000378:metabolism / Q000502:physiology / Q000503:physiopathology; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D007036:Hypothermia, Induced; D002546:Ischemic Attack, Transient / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology; D015398:Signal Transduction
D005609:Free Radicals; D016194:Receptors, N-Methyl-D-Aspartate