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

CURD

书目名称Neurochemical Correlates of Cerebral Ischemia影响因子(影响力)




书目名称Neurochemical Correlates of Cerebral Ischemia影响因子(影响力)学科排名




书目名称Neurochemical Correlates of Cerebral Ischemia网络公开度




书目名称Neurochemical Correlates of Cerebral Ischemia网络公开度学科排名




书目名称Neurochemical Correlates of Cerebral Ischemia被引频次




书目名称Neurochemical Correlates of Cerebral Ischemia被引频次学科排名




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书目名称Neurochemical Correlates of Cerebral Ischemia年度引用学科排名




书目名称Neurochemical Correlates of Cerebral Ischemia读者反馈




书目名称Neurochemical Correlates of Cerebral Ischemia读者反馈学科排名

虚度

grotto

Indebted

Disturbances of Protein and Polyamine Metabolism After Eversible Cerebral Ichemia,erves of this organ. In fact, complete cessation of blood flow in the nonanesthetized normothermic brain leads to complete depletion of energy reserves and a cessation of all endergonic metabolic processes within less than 5 min (Lowry ., 1964). However, experimental observations from our and other

optic-nerve

分散

Dysmetabolism in Lipid Brain Ischemia,e major structural component of membranes, whose integrity is a prerequisite for normal brain function. Most of the membrane phospholipids are in bilayer form, arranged with their ionic and polar heads in contact with water and with their nonpolar residues in the embedded parts (Singer and Nicolson,

合并

Involvement of Calcium, Lipolytic Enzymes, and Free Fatty Acids in Ischemic Brain Trauma,the loss of neuronal function in a time-dependent manner (Siesjö, 1981, 1984; Siesjö and Wieloch, 1985). At early stages of ischemia, recirculation of blood flow restores the energy reserves and neuronal functions, but there is a critical period of ischemia after which these functions are restored o

不安

violate

Biochemical Changes and Secondary Tissue Injury After Brain and Spinal Cord Ischemia,.., 1988). Direct effects occur acutely as a result of interruption of blood flow. Indirect effects are delayed and develop over a period of minutes to hours following the ischemic insult; this secondary injury process results, in part, from the action of endogenous biochemical factors that are acti

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