British journal of anaesthesia
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Previous studies have reported that malignant hyperthermia susceptibility is caused in some families by inherited variation in a gene located on the short arm of chromosome 19 near to, or identical with, the ryanodine receptor gene (RYR1); this is expressed in skeletal muscle as a calcium release channel of the sarcoplasm reticulum. In other families, a gene in this location is excluded, but the locations of the genes involved have not yet been defined. ⋯ The results presented here strongly suggest that the gene for malignant hyperthermia susceptibility in one or more of these three British families is located in the same region of chromosome 19q, although further work is required to decide whether or not the RYR1 gene itself is causative in these families. As genetic heterogeneity could not be excluded, we cannot yet recommend the use of DNA markers to replace in vitro contracture tests in the diagnosis of malignant hyperthermia susceptibility.
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The effect of thumb preload on adductor pollicis muscle compound action potential (ECAP) was assessed after supramaximal ulnar nerve stimulus during steady isoflurane anaesthesia in 20 ASA I-II patients without neuromuscular block. During thumb preload, the peak-to-peak amplitude of the ECAP increased by 0.9 mV, to 9.5 (SD 2.2) mV (P < 0.01), because of the increased height of the negative half-wave. ⋯ Without preload, the first dorsal interosseus muscle peak-to-peak amplitude was 13.0 (4.3) mV. Thus thumb preload may not be the solution to improved monitoring of neuromuscular block by ECAP.