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Biomedical subjects

P F Prior

Publications and source records attributed to P F Prior.

At least 37 records · Page 2Linked to original sources
PubMed1983

The use of etomidate in the management of severe head injury.

The effects of continuous and supplementary bolus dose administration of etomidate have been investigated in ten artificially ventilated patients in traumatic coma. Continuous infusion of etomidate (5-25 micrograms/kg/min) proved to be a practical and safe means of sedating these patients and appeared to control moderately elevated ICP. Additional bolus doses of etomidate (0.2 mg/kg) always reduced acutely elevated ICP (greater than 20 mmHg), which fell by a mean of 33%. However, MAP usually fell, and occasionally serious hypotension occurred. Of a total of 61 bolus dose administrations which were analysed, CPP rose on 40 occasions, fell on 19 and was unchanged twice. There was a weak correlation between the control level of ICP and the magnitude of the fall in ICP in response to the bolus dose of etomidate (r = 0.51, p less than 0.001). Bolus doses of etomidate given just before noxious stimulation, for example chest physiotherapy, prevented or limited the expected rise in ICP (with bolus mean change in ICP = -2.7 +/- 6.9 mmHg, without bolus mean change in ICP = +7.0 +/- 6.4 mmHg). Again MAP tended to fall following the bolus dose. Overall CPP tended to fall slightly following stimulation whether or not a bolus dose was administered (-3.2 +/- 11.1 mmHg and -4.9 +/- 11.5 mmHg respectively). However, when the bolus of etomidate was not given, occasional dramatic and dangerous rises in ICP were seen, in spite of the infusion, during which CPP fell to critical levels. This very rarely occurred when the bolus had been given. Furthermore, serious episodes of hypotension in response to etomidate administration appeared to occur mainly in patients who were relatively hypo-volaemic.

Adolescent↗
PubMed1980

The pathogenesis of ischaemic neuronal damage along the cerebral arterial boundary zones in Papio anubis.

The pathogenesis of ischaemic neuronal damage along the arterial boundary zones of the forebrain was investigated in 20 lightly anaesthetized, spontaneously breathing baboons. A combination of bilateral common carotid artery occlusion and systemic hypoxia was used. An arterial PO2 of 21.2 +/- 2.5 mmHg was maintained for about 20 min. Additional occlusion of the left common carotid artery for 20 min had no effect on the EEG (except for one animal with a cerebrovascular anomaly). Only when occlusion of the right carotid artery was added did the EEG become almost or completely isoelectric after an interval ranging from 23 s to 44 min (sequential common carotid artery occlusion while breathing air did not affect the EEG). After a chosen period of electrical silence, hypoxia and carotid occlusion were terminated. Hypotension did not occur during carotid occlusion or the recovery period. Survival was deliberately limited to 46 h, during which neurological assessment was made and the EEG was recorded just before in vivo perfusion-fixation of the brain. Neurological deficits included asymmetrical quadriparesis and myoclonus epilepsy. The brains of 3 animals were normal and in the 15 with brain damage this was restricted in the cerebral cortex to the arterial boundary zones. In the presence of profound hypoxia the oligaemia due to bilateral carotid occlusion can reduce tissue oxygenation locally to a level critical for the production of ischaemic damage in the cortical boundary zones. Portions of the basal ganglia were also involved in 7. The quantified brain damage scores correlated with the EEG scored on a six-point scale during the perod of electrical silence and early recovery. Brain damage scores also correlated with the times for intracranial pressure to return to normal levels from the peaks recorded just after the end of arterial occlusion and hypoxia. As brain damage only occurred when the EEG during bilateral carotid occlusion and hypoxia was silent for at least 8 min, it was concluded that in a variety of clinical settings a simple EEG-based monitoring system would be optimal for the detection of an impending failure of cerebral oxygen supply.

Animals↗
PubMed1978

Profound hypoxia in Papio anubis and Macaca mulatta--physiological and neuropathological effects. I. Abrupt exposure following normoxia. II. Abrupt exposure following moderate hypoxia.

Lightly anaesthetized and spontaneously breathing P. anubis (PA) and M. mulatta (MM) inhaled at ambient pressure 3.2% oxygen (identical to 37,500 ft or 11,430 m) from air and also after pre-exposure to 14% oxygen (identical to 10,000 ft or 3,048 m). The EEG, ECG, respiratory rate, arterial and cerebral venous sinus pressures, end-tidal pO2 and pCO2 and body temperature were recorded. Arterial and cerebral venous sinus blood gases, pH and pyruvate and lactate contents were estimated. Before hypoxia, MM showed a relative hyperventilation. Profound hypoxia, from air, ended with the "last breath" at 89--205 sec in PA and at 93--570 sec in MM. Brain damage was restricted to one MM (4 exposures). Profound hypoxia after exposure to 14% oxygen ended with the "last breath" at 87--210 sec in PA and at 120 sec--94 min (including 9 exposures over 5 min) in MM. Brain damage was restricted to one MM ("last breath" at 94 min). In the two MM with brain damage there was evidence of reduction in cerebral perfusion near the end of profound hypoxia. Brain damage in one animal contrasts with the frequent and often severe brain damage in MM after equivalent sub-atmospheric decompressions preceded by exposure to moderate altitude (10,000 ft).

Animals↗
PubMed1978

E.E.G. monitoring for the control of anaesthesia produced by the infusion of althesin in primates.

The continuous infusion of Althesin under electroencephalographic (e.e.g.) control provided a constant level of light anaesthesia for periods of 1--5.5 h during experimental brain hypoxia in spontaneously breathing baboons and Rhesus monkeys. Polygraphic records (respiration, heart rate, arterial pressure, cerebral venous sinus pressure, end-tidal gas concentrations) and also estimation of blood-gas tensions, pH, and concentrations of pyruvate and lactate demonstrated a steady physiological state. Various methods of e.e.g. monitoring were tested to establish an optimal assessment of depth of anaesthesia as a guide to the control of the rate of infusion of Althesin. A purpose-built modification of the Cerebral Function Monitor was found to give unequivocal recognition of changing depths of anaesthesia.

Alfaxalone Alfadolone Mixture↗
PubMed1977

Reversible profound depression of cerebral electrical activity in hyperthermia.

Transient major reduction of EEG activity in an hyperpyrexic patient (rectal temperature 42.5 degrees C) and transient isoelectric ECoG during accidental hyperthermia (rectal temperature 41.8 degrees C) in a Rhesus monkey are reported. Since recovery of electrocortical activity occurred in both instance this implies that in hyperthermia, as well as in hypothermia, an isoelectric EEG may not indicate irreversible brain damage.

Adult↗
PubMed1971

Monitoring cerebral function: clinical experience with new device for continuous recording of electrical activity of brain.

A device, the cerebral function monitor, provides a continuous record of the electrical activity of the brain occurring at frequencies from 2 to 15 Hz. It is relatively cheap, portable, and easy to use and interpret. The apparatus has proved of value in three circumstances: firstly, when the cerebral circulation is likely to be vulnerable during open heart surgery; secondly, as a measure of recovery or deterioration following brain damage or drug overdose; and thirdly, where information about more physiological changes in cerebral function is required, for instance when testing anaesthetic and hypnotic drugs.

Adolescent↗