Titlebook: Cerebral Blood Flow in Acute Head Injury; The Regulation of Ce Georg Emil Cold Book 1990 Springer-Verlag/Wien 1990 head.head injury.intracr

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Ischaemic Thresholds and Development of Ischaemia,extracellular space remains stable until CBF levels of 20 ml/100 g/min; below this value pH fell rapidly (Harris .. 1987) and an increase in brain water was observed (Symon .. 1979). If CBF falls to about 10 ml/100 g/min, further cytotoxic oedema occurs as a result of sodium passage into the cells.

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枯燥

Measurement and Cerebral Blood Flow and Oxygen Consumption, and the Regulation of Cerebral Circulatmplete equilibration in concentration between blood and tissue. The principle of calculation of CBF is based on the measurement of .. The technique has been developed during the last 40 years and was originally introduced by Kety and Schmidt (1945) with the use of . as tracer. Later, the technique w

Cursory

Ischaemic Thresholds and Development of Ischaemia,00 g/min and irreversible paralysis supervenes when CBF is permanently reduced to about 17–18 ml (Heiss .. 1976, Jones .. 1981). In studies of gerbils subjected to acute cerebral ischaemia by carotid ligation, a CBF threshold of CBF at 20 m1/100 g/min has been defined; below this threshold MR spectr

GLOSS

The Effect of Barbiturate and Mannitol on CBF and Metabolism,ssed. The use of Ca + + blocking agents and indomethacin will not be discussed in this review, because at present no clinical studies in patients with severe head injury are available. On the other hand, barbiturate and mannitol have been used in the control of ICP-hypertension for many years. In th

拋射物

Experimental Studies of Head Injury,rculation and metabolism. Later, the effect of mass-lesions caused by haematoma, ischaemia, brain oedema, intracranial hypertension, and systemic hypotension and hypertension may influence ICP, CBF, and CMRO.. Accordingly, studies in experimental models, including one or more of these pathogenic fac

subordinate

Human Studies of Head Injury,91%. These changes are found in the cerebral cortex in 46%, hippocampus 81%, cerebellum 36% and to the basal ganglia in 79% (Graham .. 1978). Moreover, direct impact after a blunt lesion and secondary events like hypotension might result in localized necrosis at boundary zones between the major cere

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Summary,m of this review to describe the dynamic changes in CBF, cerebral metabolic rate of oxygen (CMRO.), cerebral autoregulation (CA), and reactivity to PaCO. and barbiturate (metabolic reactivity) in the acute phase after severe head injury and to discuss the therapeutical consequences with reference to