Introduction

Malignant hyperthermia (MH) is an inherited disorder which predisposes sufferers to skeletal muscle hypercontraction, severe metabolic acidosis and a potentially lethal hyperthermia (Britt, 1985; McGrath, 1986; Sessler, 1986; O'Brien, 1987; Gronert, Mott & Lee, 1988; Harriman, 1988; Heffron, 1988; Rosenberg, 1988). In man, MH is usually triggered in susceptible individuals by halothane anaesthesia. A similar condition occurring in pigs is called the porcine stress syndrome (PSS). In response to halothane such PSS-susceptible pigs quickly develop a tachycardia and hyperventilate. Cyanotic areas then form on the skin, muscles hypercontract, limb rigidity occurs and a fatal hyperthermia ensues. Postmortem reveals oedematous, malodourous muscle with a severely disrupted structure. This meat is termed pale soft exudative (PSE) and cannot be used commercially. As well as halothane, stresses caused by transportation, exercise, feeding, mating and parturition will cause the development of a MH attack in pigs (Mitchell & Heffron, 1982).

PSS is regarded as a good model for human MH (Gronert, 1980) and has been used for much of the research into the mechanisms and causes of the disease. There is no uncomplicated and reliable diagnostic test for MH/PSS. Induction of limb rigidity by halothane inhalation will identify PSS-susceptible individuals and cause only limited mortality when performed by a skilled operator (Webb, 1980). In humans the disease is often recognised in a family when one person undergoes halothane anaesthesia prior to a surgical procedure. Thereafter muscle samples from other members of the family can be subjected to in vitro contracture tests to identify abnormal reaction to either halothane or caffeine.