Titlebook: Neurochemical Correlates of Cerebral Ischemia; Nicolas G. Bazan,Pierre Braquet,Myron D. Ginsberg Book 1992 Springer Science+Business Media

Accommodation

Dysmetabolism in Lipid Brain Ischemia,nal transmission or transduction. Considering the pathogenetic mechanism of ischemic cell damage as membrane injury, it is quite reasonable to assume that the alterations in lipid metabolism during and after brain ischemia are closely related to ischemic brain damage.

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Metabolic Correlates of Focal Ischemia,mpounded by an incomplete understanding of the control mechanisms regulating blood flow of the brain under normal and pathological conditions. Our working hypothesis is that the normal coupling mechanisms among function, blood flow, and metabolism are perturbed during and after ischemia and, further

替代品

Role of Pyruvate Dehydrogenase in Ischemic Injury,. have been postulated, but definitive proof implicating a specific target in cellular injury is lacking. Indeed, a causative relationship between increased [Ca]. and ischemic injury has not been established (Siesjö, 1988).

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Disturbances of Protein and Polyamine Metabolism After Eversible Cerebral Ichemia, of the brain (Schmidt-Kastner ., 1986). Most ischemic experiments exceeding a duration of 5 to 10 min nevertheless result in more or less severe brain injury when the animals are allowed to survive for some time (Siesjö, 1988.). The foci of ischemic cell injury are accentuated in the so-called sele

Conspiracy

Oxygen Dependence of Neuronal Metabolism,ization with attendant increased intracellular Ca. levels, and release of neurotransmitters such as the excitatory amino acids. After longer periods (minutes) there is progressive lipolysis and proteolysis. In the first minutes of this process it may be fully reversible, and reoxygenation leads to e

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Involvement of Calcium, Lipolytic Enzymes, and Free Fatty Acids in Ischemic Brain Trauma,role in ischemic injury (Siesjö, 1990; Bazan, 1976; Bazan ., 1986). Several studies have indicated that ischemic insult markedly affects membrane integrity and membrane-associated functions such as activities of membrane-bound enzymes, ion transport, oxidative phosphorylation, and synaptic transmiss

incite

Arachidonic Acid Lipoxygenase Products Participate in the Pathogenesis of Delayed Cerebral Ischemiaides, particularly thiobarbituric acid-reactive substance (TBA-RS), was significantly higher in SAH patients who manifested symptoms of vasospasm than in those who did not (Sasaki ., 1982). Furthermore, the elevation of the CSF level of TBA-RS in SAH patients was found to be accompanied by a decreas

结束

Biochemical Changes and Secondary Tissue Injury After Brain and Spinal Cord Ischemia, Rothman and Olney, 1986), and opioid peptides (Faden, 1990). It is likely that the effects of a number of these factors are interactive, with ultimate tissue damage resulting from a complex multifactorial process.

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