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Experimental cerebral 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]

Corbett D. and Nurse S. (1998) The problem of assessing effective neuroprotection in experimental cerebral ischemia. Prog. Neurobiol. 54,531-548. [Pg.13]

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]

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]

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]

In addition to the MCAO-induced focal ischemia model, other in vivo experimental cerebral ischemia models were employed to examine the activities of 30. Compound 30 was protective against cerebral damage induced by 4-vessel occlusion (experimental cerebral ischemia secondary to cardiac failure) [324, 325], physical closed head injury [326, 327], and subarachnoid hemorrhage [328-330] (Table 4). [Pg.646]

Namura S, Zhu J, Fink K, Endres M, Srinivasan A, TomaseUi KJ, Yuan J, Moskowitz MA. Activation and cleavage of caspase-3 in apoptosis induced by experimental cerebral ischemia. J Neurosci. 1998 18 3659-3668... [Pg.17]

Recent studies have shown that phototherapy as a nondrug treatment for ischemic stroke. According to recent studies on near infrared laser therapy (NILT), the time window of treatment could be extended to more than 24 hours in contrast to neuroprotection drugs [6, 7]. In this pilot study, we intend to develop an integrated NIR assessment and NILT treatment system that could noninvasively monitor the dysfunction and abnormality of brain function under experimental cerebral ischemia. [Pg.600]

Hossmann, K. A., 1982 Treatment of experimental cerebral ischemia. J. Cereb. Blood Flow Metab. 2, 275-297. [Pg.76]


See other pages where Experimental cerebral ischemia is mentioned: [Pg.238]    [Pg.388]    [Pg.30]    [Pg.69]    [Pg.132]    [Pg.146]    [Pg.79]    [Pg.163]    [Pg.167]    [Pg.190]    [Pg.450]    [Pg.197]   
See also in sourсe #XX -- [ Pg.197 ]




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