Abstract
The syndrome of malignant hyperthermia (MHS) has been visualized from the point at which sarcoplasmic Ca2+ concentration becomes sufficient to stimulate phosphorylase kinase and, indirectly, myosin ATPase. Elevated levels of cellular Ca2+ may cause a functional uncoupling of oxidative phosphorylation as the mitochondria utilize high energy intermediates to sequester Ca2+. Consequently, ATP is consumed, and the cellular levels of ADP and inorganic phosphorus increases, further stimulating glycolysis as the MHS develops. As the mitochondria sequester Ca2+, O2 consumption is increased and this, in addition to the stimulating effect of temperature, may explain the observed increase in O2 consumption. However, the triggering mechanisms that allow the various body functions, when exposed to halothane, to combine in an abnormal manner to produce what we recognize as malignant hyperthermia remain obscure. Copyright © 1975. American Society of Animal Science . Copyright 1975 by American Society of Animal Science.