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In a report of two patients who died of malignant hyperthermia, muscle adenylate kinase deficiency was identified in the father and brother of the deceased. To determine if this enzyme deficiency was a biochemical marker for susceptibility to malignant hyperthermia, we measured adenylate kinase in
Blood platelets from malignant hyperthermia patients share the same defect as skeletal muscle. This could be verified by the effect of halothane on the energy metabolism of blood platelets under optimal experimental conditions. The sensitivity of changes in adenine nucleotide metabolization to
The key factor in malignant hyperthermia does not seem to be a defect in the calcium-storing membrane of the skeletal and cardiac muscle cells. The primary cause would appear to be deficiency of adenylate kinase.
Muscle biopsies from 35 patients referred for possible malignant hyperthermia were subjected to contracture testing with halothane, caffeine, and the combined agents, histopathological and fiber-type-distribution analysis, and quantitative assay of three major muscle enzymes: adenylate deaminase,
The effects of an induced malignant hyperthermia (MH) crisis have been studied in the intact pig. Both physiological and biochemical changes in skeletal muscle were studied. MH was induced with 3% halothane plus a bolus injection of succinylcholine. In the prechallenge period a significant
Several biochemical markers in the cerebrospinal fluid (CSF) of 120 patients with serous meningoencephalitis (SM) of viral origin were compared with those of 74 patients with viral or bacterial infections accompanied by neck stiffness but no CSF abnormality (i.e., meningism). CSF adenylate kinase