Titlebook: Mechanisms of Cerebral Hypoxia and Stroke; George Somjen Book 1988 Plenum Press, New York 1988 brain.cell.cell death.cortex.oxygen.paper.p

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Microcirculation, NAD/NADH Fluorescence, Extracellular Potassium and Glucose Metabolism Changes in FThe cerebral tissue is very sensitive to interruption of oxygen and substrate supply. In the present study we examined the changes of cerebral electrical activity (ECoG), cerebrocortical blood flow, extracellular potassium concentration ([K.].), NAD/NADH redox state and glucose metabolic rate (CMRg1) in a focal cerebral ischemia model in the cat.

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Perigee

特別容易碎

https://doi.org/10.1007/978-1-4684-5562-5brain; cell; cell death; cortex; oxygen; paper; physiology; receptor; tissue

Minikin

Pathology of Ischaemic Brain Damage — Implications for Therapyter a stroke. The second important step in the treatment of acute stroke is inhibition of blood platelet aggregation to arrest the thrombotic process and avoid complete occlusion of the artery, or in the case of an embolism to limit the extent of the infarct.

幼稚

Cerebral Hypoxia during Repetitive Seizurestatus epilepticus (e.g., pulmonary edema) also can profoundly decrease cerebral oxygenation. An important remaining question is whether the cerebral hypoxia accompanying later seizures contributes to the neuronal damage following prolonged status epilepticus.

Control-Group

ellagic-acid

Cantankerous

Cerebral Blood flow and Its Responsiveness to CO2 after Traumatic and Ischemic Brain Injuries tissue electric impedance (cf refs 1,2). Measurements by REG roughly matched those by H. clearance. Measurements were made while the animal was breathing room air and also during 7% CO. inhalation, which raised PaCO. by 6–8 mmHg Responsiveness to CO. was quantified as the ratio of rCBF with and without elevated PaCO..

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