Membrane Permeability in Porcine Malignant Hyperthermia

Abstract

Malignant hyperthermia syndrome can be induced in stress-susceptible pigs by anaesthesia with halothane (Harrison et al., 1968; Berman et al., 1970; Nelson et al., 1972; Hall et al., 1972; Gronert and Theye, 1976). The predominant clinical symptoms of this syndrome are gross muscular rigidity, rapid rise in body temperature, tachycardia, hyperventilation, severe metabolic acidosis and elevated levels of serum metabolites (Brucker et al., 1973; van den Hende et al., 1976). The genetic inheritance was suggested to be due either to a single autosomal dominant gene with incomplete penetrance (Hall et al., 1966), or to an autosomal recessive gene with variable penetrance (Christian, 1972) or to a single recessive gene with incomplete (Ollivier et al., 1975) or compelte (Eikelenboom et al., 1978) penetrance. In spite of the well documented etiology of porcine malignant hyperthermia syndrome the lesion responsible for the series of biochemical events leading to this syndrome is unknown. The inherent defects are not apparently confined to skeletal muscle, as it is believed that neuronal and hormonal abnormalities (LaCour et al., 1971) may also exist.