F. Colbourne et al., POSTISCHEMIC HYPOTHERMIA - A CRITICAL-APPRAISAL WITH IMPLICATIONS FORCLINICAL TREATMENT, Molecular neurobiology, 14(3), 1997, pp. 171-201
The use of hypothermia to mitigate cerebral ischemic injury is not new
. From early studies, it has been clear that cooling is remarkably neu
roprotective when applied during global or focal ischemia. In contrast
, the value of postischemic cooling is typically viewed with skepticis
m because of early clinical difficulties and conflicting animal data.
However, more recent rodent experiments have shown that a protracted r
eduction in temperature of only a few degrees Celsius can provide sust
ained behavioral and histological neuroprotection. Conversely, brief o
r very mild hypothermia may only delay neuronal damage. Accordingly, p
rotracted hypothermia of 32-34 degrees C may be beneficial following a
cute clinical stroke. A thorough mechanistic understanding of postisch
emic 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 thi
s article is to evaluate critically the effects of postischemic temper
ature changes with a comparison to some current drug therapies. This a
rticle will stimulate new research into the mechanisms of lengthy post
ischemic hypothermia and its potential as a therapy for stroke patient
s.