Titlebook: Cerebral Ischemia and Basic Mechanisms; Alexander Hartmann,Frank Yatsu,Wolfgang Kuschinsky Conference proceedings 1994 Springer-Verlag Ber

Priapism

Effects of Extracellular Acidosis on Glial Cell Intracellular pH: Evidence for a Glial Spatial H+-Buseizures,, and head injury (Siesjo 1981). A marked decrease in brain tissue pH has been demonstrated in cerebral ischemia - even more so in hyperglycemic subjects - where lactic acid may accumulate to 20–30 mM and higher concentrations (Rehncrona et al. 1980; Katsura et al. 1991). Tissue pH may drop

amyloid

Calcium Channel Blockers Prevent Delayed Cerebral Ischemia After Intracranial Aneurysmal Subarachnoirough endothelial and ischemic neuronal cell membranes [9, 30]. It is well known that when Ca. ions enter vascular smooth muscle, contraction results, but if calcium entry is blocked by calcium antagonists, vascular dilatation occurs. It is also well known that when extracellular Ca2+ moves into isc

终止

Monosialoganglioside GM1 in Experimental Models of Strokelevels of glutamate accumulate in the interstitial fluid during an ischemic/traumatic episode [3] and, through the activation of ionotropic glutamate receptors, initiate a cascade of cellular events which ultimately lead to irreversible cell damage. These cellular events contributing to excitotoxici

有效

What Are We Learning from Clinical Trials in Acute Cerebral Ischemia?chemia, such as osmotics, steroids, vasodilators, hemodilution, which have all systematically failed. We would rather not elaborate that discouraging list but think about how to make use of these negative experiences as examples of methodological errors which should not be repeated. Thus, studies wi

acquisition

Threshold of Calcium Influx After Global and Focal Ischemia: Implications for the Window of Therapeuum [13, 14]. Activation of calcium-dependent enzymes such as protein kinase C, calmodulin (CaM) kinase II, calpain I, calcineurin, and phospholipase A2 is believed to play a major role in neuronal excitotoxicity [2, 4, 5, 16]. In addition, therapeutic intervention with agents which target either vol

frivolous

确认

Oberrheinische Studien Band III but this depends to some extent on the definition of the term; it is useful and less nihilistic to take a broader view. In the past two decades much evidence has accumulated on the many parameters which define this window, or rather these windows.

伟大

https://doi.org/10.1007/978-3-662-24747-1tive for different therapeutic approaches: one short period during which improvement of perfusion is successful in reversing functional deficits and preventing morphological damage, and a probably longer period during which the progressive infarction could be ameliorated by intervention with ongoing

Incise

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