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Query: UMLS:C0024591 (malignant hyperthermia)
 2,353 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is generally assumed that the brain is not primarily involved in the development of a malignant hyperthermia syndrome (MH). However, spontaneous brain electrical activity (EEG) has not been related temporally to the development of haemodynamic, respiratory and metabolic changes during a fulminant MH crisis. In the present study cerebral blood flow (CBF) and spontaneous electroencephalogram (EEG) were recorded in 8 pigs susceptible (MHS) for the development of malignant hyperthermia and 8 non-susceptible pigs (nMHS) after exposure to 1% halothane. Power densities in selected frequency bands were calculated from the EEG. Additionally, body temperature and haemodynamic and blood gas parameters were studied over a period of 60 min. MH was triggered in all MHS animals. Following exposure to halothane initial EEG changes were noted after 20 to 30 min. They consisted of a decrease in total power and a shift to lower frequencies (delta-theta activity). At this time, CBF was significantly increased compared to control. In 4 animals an isoelectric EEG was noted at a PaO2 of 65-78 mmHg and PaCO2 of 52 to 64 mmHg. Characteristic changes for the development of an MH syndrome in haemodynamic and respiratory parameters as well as a rise in body temperature occurred after first EEG changes were seen. Our results do not support the hypothesis that early EEG changes during MH occur as a result of systemic hypotension, hypoxaemia, hypercapnia or cerebral ischaemia. Our data indicate that EEG monitoring in combination with monitoring of haemodynamic, respiratory and metabolic parameters may be of value for an early detection of an MH-crisis.
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PMID:[Characteristics of cerebral blood flow and the electroencephalogram during experimental malignant hyperthermia]. 225 75

Intracellular free calcium is believed to play a major role in the ischaemic cascade which leads to cell death. Calcium channel blockers, which in part inhibit the influx of extracellular calcium, have been shown to be neuroprotective in both complete and focal cerebral ischaemia models. Dantrolene, an agent used in the treatment of malignant hyperthermia, is known to inhibit the release of stored intracellular calcium. Assuming that reduced levels of intracellular free calcium would improve neurologic outcome, we studied the neuroprotective potential of dantrolene. A complete cerebral ischaemia model was used to examine ten anesthetized dogs. Five were given intravenous dantrolene and five were given equal volumes of saline prior to the ischaemic event. Simultaneous occlusion of the venae cavae and ascending aorta provided eleven minutes of complete cerebral ischaemia as monitored by electroencephalography. Arterial blood gases and serum glucose levels were drawn prior to ischaemia, 5 and 20 minutes post-ischaemia, and following extubation. Forty-eight hours following the ischaemic event, neurologic outcomes were scored. No significant differences were observed between the two groups. All ten dogs had equally significant increases in serum glucose levels at 5 and 20 minutes post-ischaemia. The average neurologic outcome of the five dantrolene-treated dogs equalled the average of the five controls. These results suggest that dantrolene, alone, is not neuroprotective during complete cerebral ischaemia.
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PMID:No dantrolene protection in a dog model of complete cerebral ischaemia. 809 51