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Biomedical subjects

J Calverley

Publications and source records attributed to J Calverley.

7 recordsLinked to original sources
PubMed1982

Anterior spinal artery syndrome with chronic traumatic aortic aneurysm.

Shortly after severe blunt chest trauma, a young man experienced neurological symptoms suggestive of a spinal cord lesion at the lower thoracic level. The symptoms resolved at first, but then recurred 3 years later and progressed slowly. Neurological workup failed to define the cause until a thoracic aortogram showed an aneurysm in the middle portion of the descending aorta in close proximity to a vessel supplying the anterior spinal artery. After the operative repair with precautions taken to avoid further neurological injury, the neurologic deficit resolved partially. Because of the potential for symptomatic spinal cord ischemia resulting from lesions of the aorta, angiographic delineation of the spinal cord blood supply is valuable in planning operative repair.

Adult↗
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↗
PubMed1976

Cyanide intoxication in the rat: physiological and neuropathological aspects.

Sodium cyanide was given to rats by intravenous infusion at a rate that would avert apnoea (the first sign of overdosage) in the majority. There was full physiological monitoring in a group under anaesthesia and more limited monitoring in an unanaesthetized group. White matter was damaged in six animals and grey matter additionally in only one. It was concluded that cyanide can damage neurones only through the medium of secondary effects on circulation and respiration.

Animals↗
PubMedDate not supplied

Cyanide intoxication in Macaca mulatta. Physiological and neuropathological aspects.

Sodium cyanide was infused intravenously in 11 lightly anaesthetised and spontaneously breathing M. mulatta. In most, the EEG, ECG, respiratory rate, blood pressure, cerebral venous sinus pressure, end-tidal pCO2 and body temperature were recorded. Blood gases, pH, lactate and pyruvate were estimated in arterial and venous sinus blood samples. There was an initial hyperventilation with tetany in all animals. A rapid rate of cyanide infusion led to apnoea. An isoelectric or near-isoelectric EEG was usually precipitated by bradycardia often with additional hypotension. Neither epileptic seizures nor their EEG concomitants were seen at any stage. Three animals died of early heart failure. Brain damage was seen in 4 animals surviving up to 98 hr. White matter was involved in all. Ischaemic neuronal alterations, restricted to the striatum of one animal, were attributed to major circulatory complications. It was concluded that under these experimental conditions there is no evidence for hypoxic neuronal damage of purely histotoxic type.

Animals↗