It is now recognized that skeletal muscle is the principle tissue involved in a malignant hyperthermia reaction. The demonstration by K,alo,w,i1,9Z..0) that malignant-hyperthermia-susceptible muscle developed spasm at lower concentrations of caffeine, which enhances the release of Ca 2+ from the sarcoplasmic reticulum, than muscle that was not susceptible to malignant hyperthermia laid a basis for the pathophysiology of malignant hyperthermia as well as a screening test for this condition in humans. It was proposed that the deregulation of Ca 2+ within the muscle cell could account for many of the signs in malignant hyperthermia. However, calcium is ubiquitous within the muscle cell and the exact site of the defect remains debatable. An increase in intracellular Ca 2+ could come about by increased release from or decreased uptake by the sarcoplasmic reticulum, increased release from the mitochondria, or an increase in the entry of extracellular Ca 2+ through the sarcolemma.

Whatever the source, the increase in Ca2+ in the sarcoplasm during a malignant hyperthermia reaction results in severe metabolic disturbances due to activation of the contractile proteins causing the contracture seen in malignant hyperthermia.

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