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Biomedical subjects

E Escuret

Publications and source records attributed to E Escuret.

24 records · Page 2Linked to original sources
PubMedDate not supplied

[Effects of drugs used in anaesthesia and in neurosurgical intensive care on the blood flow and metabolism of the brain (author's transl)].

Changes in cerebral blood flow (CBF) and in O2 consumption caused by anaesthetic agents were studied in 36 subjects in coma after cranial trauma. These changes can be divided into 3 groups: (1) Reduction in CBF and in O2 consumption of about the same percentage, after penthiobarbital, gamma-OH and alfathesin. (2) A reduction in CBF greater than in O2 consumption after diazepam and chlorpromazine. (3) Increase in CBF without significant change in O2 consumption after ketamine. The haemodynamic changes occur in the same direction whatever the initial value of the CBF (normal, hypoperfusion or hyperaemia). The reduction in CBF caused by gamma-OH is associated with a decrease in the arterio-venous difference in O2 (DAVO2). Gamma-OH also prevents the increase in DAVO2 observed in hypocapnia provoked by hyperventilation. These properties are an indication for using gamma-OH, alone or associated with hyperventilation, in reactive cerebral hyperaemia. Comparison of the E.E.G., CBF and cerebral O2 consumption shows that the E.E.G. changes produced by anaesthetic agents, such as fast spindles and burst suppression, are not related to any particular haemodynamic or metabolic state. The E.E.G. changes induced by penthiobarbital or diazepam can be corrected, at the same time as changes in CBF and O2 consumption, by injecting doxapram.

Alfaxalone Alfadolone Mixture↗
PubMedDate not supplied

[The effect of gamma-OH on cerebral metabolism and blood flow in human patients (author's transl)].

The effects of gamma-OH on cerebral blood flow (CBF) and metabolism were analysed in 10 neurosurgical patients, 15 min after a 60 mg/kg injection, both blood flow and oxygen consumption demonstrates a disconnection between blood flow and metabolism which appears an advantage and hence the interest in using this agent in anaesthesia and neurosurgical intensive care. 1 h40 min later no rebound effect was found; the metabolic reduction persisted whereas the CBF had returned to its resting level. Under gamma-OH CO2 production does not parallel O2 consumption and this could be interpreted as a sign that glucose-6-phosphate is metabolising via pentose.

Adolescent↗
PubMedDate not supplied

[A polygraphic, haemodynamic and metabolic study of 2 cases of the "locked-in" syndrome (author's transl)].

The sleep-waking pattern, cerebral blood flow (CBF) and cerebral metabolism have been studied in 2 cases of the "locked-in" syndrome, one traumatic, the other vascular in origin. Studies were performed in the third week in the first case and the seventh in the second. A lesion of the ventral pons was suggested clinically and neuroradiologically. The waking EEG was composed of alpha and theta activity. Different stages of slow wave sleep were diminished in quantity (NREM) as was paradoxical sleep (REM). The basal cerebral blood flow (CBF) was increased by 30 p. 100 compared to normals. Cerebral oxygen consumption was normal. The cerebral hyperaemia was evenly distributed and was associated with a failure of autoregulation. The vascular response to CO2 was normal, however. The E.E.G. findings, haemodynamic and metabolic studies confirmed a pontine lesion as the cause of the "locked-in" syndrome in contrast to akinetic mutism where the lesion is in the mid-brain.

Adolescent↗
PubMedDate not supplied

[Hemodynamic and metabolic changes at various levels of cerebral dysfunction during severe traumatic coma (author's transl)].

Cerebral blood flow (DSC) and oxygen consumption were measured in a series of patients in the acute phase of severe brain injury, and the results analyzed as a function of the level of cerebral dysfunction determined clinically. The most frequent modifications were increased cerebral blood flow and reduced oxygen consumption, whatever the degree of dysfunction. Hemodynamic data has no prognostic value whereas oxygen consumption results are more valid. Increased cerebral blood flow is noted constantly in patients at a level of mesencephalic dysfunction. Reduced O2 consumption associated with increased blood flow is the result of a disturbance in the blood flow-metabolism ratio and could be due to cerebral vasodilatation. This great increase in cerebral vasodilatation observed in cerebral dysfunction syndromes is in favour of the existence of a central neurogenic system in the brain stem regulating cerebral blood circulation.

Brain↗