Abstract
THE syndrome of malignant hyperthermia can be induced in susceptible humans1 and pigs by a variety of agents, such as halothane2 and succinyl choline3. In swine, the syndrome is well documented4–6 and its onset is characterized by a sharp rise in body temperature which is often associated with muscle rigor. One of the most interesting biochemical responses in hyperthermia is the progressive loss of muscle ATP7 and/or creatine phosphate8 and the concomitant accumulation of Pi in the blood5.
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