Catecholamine Stimulation of Myocardial Oxygen Consumption in Porcine Malignant Hyperthermia

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Abstract
Malignant hyperthermia [similar in man and swine] is a known disorder of skeletal muscle, and probably involves other organs and tissues. Because cardiac muscle is in some ways similar to skeletal muscle and because of clinical reports suggesting that cardiomyopathies run in susceptible families, malignant hyperthermia may also involve cardiac muscle. To evaluate this, myocardial O2 consumption was measured during malignant hyperthermia in 16 Poland China swine undergoing right-heart bypass. The progress of malignant hyperthermia was evaluated by determinations of whole-body O2 consumption, lactate, K and catecholamine values and acid-base balance. Ten genetically susceptible swine, 5 of which received propranolol, 40 .mu.g/kg per min, continuously i.v., were given halothane, 1% and succinylcholine, 3 mg/kg, to initiate malignant hyperthermia. Six normal swine, 1 of which received the same dose of propranolol, were also given halothane and succinylcholine to obtain control data. During malignant hyperthermia without propranolol, mean myocardial O2 consumption increased from 7 to 34 ml O2/min per 100 g heart. Swine given propranolol did not have increased myocardial O2 consumption during malignant hyperthermia, but had myocardial oxygen consumption values similar to those of normal swine with or without propranolol. During malignant hyperthermia, the myocardium did not release either lactate or K. Porcine malignant hyperthermia increases myocardial metabolism secondary to .beta.-adrenergic receptor stimulation due to increased release of catecholamines; it is unlikely that the myocardium is primarily involved in malignant hyperthermia.