Titlebook: Brain Failure; David Bihari,John W. Holaday Conference proceedings 1989 Springer-Verlag Berlin Heidelberg 1989 Nervous System.Sepsis.Traum

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https://doi.org/10.1007/978-1-4842-6543-7is for a few moments. The amount of lactic acid accumulation is primarily dependent upon the preischemia tissue glucose stores, which are proportional to the blood glucose concentration. After 2–3 min, ATP stores become depleted, and the adeny-late energy charge reaches minimal values after approximately 5 min.

晚間

https://doi.org/10.1007/978-1-4842-6543-7ay develop symptoms ranging from mild sensorial clouding to delirium and coma [2]. Even after the institution of adequate maintenance dialysis therapy, patients may continue to manifest more subtle nervous system dysfunction such as impaired mentation, generalized weakness, sexual dysfunction and peripheral neuropathy [3, 4].

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The Role of Lipid Peroxidation in Ischemic Central Nervous System Injury,ethods of measurement. Until then, evidence to support lipid peroxidation as a mediator of tissue injury will rely largely on current methods of detection and experimental observations that pharmacologie antagonism of oxygen radical generation and/or lipid peroxidation results in a therapeutic effect.

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Pathophysiology of the Encephalopathies Associated with Uremia and Hyponatremia,ay develop symptoms ranging from mild sensorial clouding to delirium and coma [2]. Even after the institution of adequate maintenance dialysis therapy, patients may continue to manifest more subtle nervous system dysfunction such as impaired mentation, generalized weakness, sexual dysfunction and peripheral neuropathy [3, 4].

引起

Drug-Induced Encephalopathy,n hospitalized patients, particularly the elderly, disturbances in cerebral function due to a wide range of causes are common, and drugs may be more than just a superficial component of such adverse events.

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連詞

Moritz Veckenstedt,Randjbar Vitzthumrt by an excess release of glutamate, leading to over-activity at synapses utilizing excitatory amino acid transmitters [3, 4]. Glutamate antagonists able to penetrate CNS might, thus, have considerable therapeutic potential. In particular, the NMDA receptor subtype [5, 6] seems to be a key target,

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