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Mild hypothermia ischemia

Markarian GZ, Lee JH, Stein DJ, Hong SC. Mild hypothermia therapeutic window after experimental cerebral ischemia. Neurosurgery 1996 38 542-550 [discussion 551]. [Pg.119]

In 1987, however, a study by Busto et al. (5) showed that small decreases in brain temperature (as little as 2-5°C below normal brain temperature) conferred a marked protective effect against experimental global cerebral ischemia. This finding, as well as subsequent animal studies that modeled neurodegenerative diseases and CNS injury, led to a resurgence of interest in mild hypothermia as a method of cerebral protection. [Pg.2]

Chopp M., Knight R., Tidwell C. D., Helpern J. A., Brown E., and Welch K. M. (1989) The metabolic effects of mild hypothermia on global cerebral ischemia and recirculation in the cat comparison to normothermia and hyperthermia. J. Cereb. Blood Flow Metab. 9, 141-148. [Pg.12]

Busto R., Globus M. Y., Dietrich W. D., Martinez E., Valdes I., and Ginsberg M. D. (1989) Effect of mild hypothermia on ischemia-induced release of neurotransmitters and free fatty acids in rat brain. Stroke 20, 904-910. [Pg.12]

Maier C. M., Sun G. H., Cheng D., Yenari M. A., Chan P. H., and Steinberg G. K. (2002) Effects of mild hypothermia on superoxide anion production, superoxide dismutase expression, and activity following transient focal cerebral ischemia. Neurobiol. Dis. 11, 28 -2. [Pg.13]

Similarly, following 10 min of forebrain ischemia, mild hypothermia applied for 3 h attenuated apoptotic death in hippocampal neurons 72 h postinsult (119). The neuroprotection appeared to be correlated with increased expression of Bcl-2, an antiapoptotic protein. [Pg.30]

Colbourne F., Li H., and Buchan A. M. (1999) Indefatigable CA1 sector neuroprotection with mild hypothermia induced 6 hours after severe forebrain ischemia in rats. J. Cereb. Blood Flow Metab. 19, 742-749. [Pg.34]

Graf R., Matsumoto K., RisseF., RosnerG., andHeiss W. D. (1992) Effect of mild hypothermia on glutamate accumulation in cat focal ischemia. Stroke 23, 150. [Pg.36]

Mild Hypothermia in Experimental Focal Cerebral Ischemia... [Pg.39]

The mechanisms whereby brain cells die during ischemia are not fully understood. Experimental evidence points to a complex array of parallel hemodynamic, biochemical, and electrophysiological events that combine to produce neuronal damage. In experimental cerebral ischemia, the severity of this damage can be significantly reduced by treatment with mild hypothermia (2-5°C below normal brain temperature). [Pg.39]

The concept of neuroprotection relies on the fact that delayed neuronal injury occurs after ischemia, and each step along the ischemic cascade provides a target for therapeutic intervention. Thus, understanding the cellular and molecular mechanisms that underlie the development of neuronal and vascular injury is critical to optimize treatment. This chapter reviews experimental evidence from studies on focal cerebral ischemia and mild hypothermia, as well as the mechanisms involved in mild hypothermic neuroprotection. [Pg.40]

Mild hypothermia has been shown to reduce neurological deficits if started before, during, or after cerebral ischemia, but few studies have examined functional outcome in detail after experimental cerebral ischemia with hypothermia (29-33). [Pg.49]

We recently carried out a study (40) to determine the effects of delaying induction of mild hypothermia after transient focal cerebral ischemia and to ascertain whether the neuroprotective effects of mild hypothermia induced during the ischemic period are sustained over... [Pg.50]

The main role of mild hypothermia against stroke may, perhaps, be to extend the therapeutic window of other treatment modalities. On the other hand, hypothermia is by far the most potent neuroprotectant available against experimental cerebral ischemia, and new technological advances are now facilitating its implementation in the clinical setting. Understanding the mechanisms by which mild hypothermia exerts its neuroprotective effects will allow us to optimize its use as a therapeutic strategy. [Pg.52]

When mild hypothermia was first shown to be beneficial, the assumption was that a substantial portion of its neuroprotective effect stemmed from a reduction in cerebral metabolism. However, studies on cerebral metabolic rate (CMR) made it clear that the degree of neuro-pathological injury following ischemia with mild hypothermic treatment did not correlate with the magnitude of metabolic depression observed (42). A reduction in temperature from 37°C to 34°C produces a 15-20% reduction in cerebral metabolism (approx 5-7% per °C), which is far less than the 50% decrease seen with electroencephalogram (EEG) silence. Furthermore, reductions in metabolism produced by anesthetics vs hypothermia are not equally neuroprotective (43). Thus, hypothermic neuroprotection cannot be explained by alterations in metabolic rate alone. [Pg.52]

Neurotransmitters such as glutamate interact with a variety of receptors that are coupled to second messenger systems. The effects of mild hypothermia on ischemia-induced changes in intracellular messenger systems and mediators have also been studied and are described in Chapter 2. [Pg.53]

To examine the effects of mild hypothermia on the cellular and molecular events associated with the production of ROS implicated in ischemia-induced neuronal damage, we have used a 2-h MCAO model and survival times up to 2 mo postinsult (4). By means of free radical fluorescence, we have shown that mild intraischemic hypothermia significantly reduces the generation of superoxide (02 ), a free radical that is directly toxic to neurons (76), in peri-infarct areas. We have also shown that 02 is produced primarily in neurons and endothelial cells, although some 02- production is occasionally observed in oligodendrocytes with this model. [Pg.55]

Huang F. and Zhou L. (1998) Effect of mild hypothermia on the changes of cerebral blood flow, brain blood barrier and neuronal injuries following reperfusion of focal cerebral ischemia in rats. Chin. Med. J. (Engl.) Ill, 368-372. [Pg.61]

Huang F. P., Zhou L. F., and Yang G. Y. (1998) Effects of mild hypothermia on the release of regional glutamate and glycine during extended transient focal cerebral ischemia in rats. Neurochem. Res. 23,991-996. [Pg.61]

MaierC., Tannous N., Steinberg G., and Chan P. (2001) Increased rate of hemorrhage in SOD2-deficient mice after transient focal cerebral ischemia effect of mild hypothermia. Neurology 56, A305. [Pg.63]

There have been few reports on the effects of temperature on brain ion homeostasis after ischemia. However, there appears to be a consensus that hypothermia does not prevent AD associated with either global or focal ischemia, although it has been reported that the onset of AD may be delayed (32-34). It has also been reported that mild hypothermia reduces the number of SD-like depolarizations associated with focal ischemia (34). The frequency of SD-like depolarizations has been associated with the degree of damage after focal ischemia (35,36). It is possible that the same occurs following TBI. [Pg.70]


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See also in sourсe #XX -- [ Pg.39 , Pg.40 , Pg.41 , Pg.42 , Pg.43 , Pg.44 , Pg.45 , Pg.46 , Pg.47 , Pg.48 , Pg.49 , Pg.50 , Pg.51 , Pg.52 , Pg.53 , Pg.54 , Pg.55 , Pg.56 ]




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Mild hypothermia

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