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

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https://doi.org/10.1007/978-3-662-28348-6list but think about how to make use of these negative experiences as examples of methodological errors which should not be repeated. Thus, studies with a poor diagnostic characterization of patients due to the lack of a computed tomography (CT) scan and trials carried out using insufficient sample sizes should never be performed.
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Effects of Extracellular Acidosis on Glial Cell Intracellular pH: Evidence for a Glial Spatial H+-Bumic 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 to pH 5.5 (Chopp et al. 1988). In consequence, acidosis has since long been suspected as a mediator of brain damage (Siesjö 1981).
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What Are We Learning from Clinical Trials in Acute Cerebral Ischemia?list but think about how to make use of these negative experiences as examples of methodological errors which should not be repeated. Thus, studies with a poor diagnostic characterization of patients due to the lack of a computed tomography (CT) scan and trials carried out using insufficient sample sizes should never be performed.
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Conference proceedings 1994ational conference on Cerebral Ischemia and Basic Mechanisms held in Bad Schachen/Lake Constance, Germany in June 1992. The enormous progress in research recently on the basic mechanisms associated with cerebral ischemia has provided greater insight into the pathophysiological mechanisms of reduced
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https://doi.org/10.1007/978-3-662-26794-3tracellular messengers and mitochondrial metabolism [31]. Experimental studies of cerebral ischemia in animal models have shown that pretreatment with the calcium entry antagonist nimodipine results in protection of the brain from cerbral infarction by preventing calcium entry into ischemic neurones and glia [1].
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Otfrid Foerster · Arzt und Naturforscher delay providing a potential window of opportunity for therapeutic intervention. Thus, understanding these processes seems to offer hope for the more effective treatment of brain ischemia and stroke [13].
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Uncoupling of Flow and Metabolism in Early Ischemic Strokel setting, however, is extremely difficult since most routine examinations do not yield evidence for viability of tissue, and regional studies of physiologic variables, for example, by positron emission tomography (PET) are prevented in most instances by their logistic complexity.
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