Key result
Propranolol prevented the increase in myocardial oxygen consumption during malignant hyperthermia in susceptible swine.
Why the study?
Does propranolol prevent the increase in myocardial oxygen consumption during malignant hyperthermia in susceptible swine?
Does propranolol prevent the increase in myocardial oxygen consumption during malignant hyperthermia in susceptible swine?
Porcine malignant hyperthermia increases myocardial metabolism secondary to beta-adrenergic receptor stimulation, suggesting the myocardium is not primarily involved in the disorder.
Answers are grounded in this paper and cite their sources.
Does not change clinical management of malignant hyperthermia; hypothesis-generating for beta-adrenergic mechanisms in porcine model.
Malignant hyperthermia, a known disorder of skeletal muscle, probably also involves other organs and tissues. Because cardiac muscle is in some ways similar to skeletal muscle and because of clinical reports suggesting cardiomyopathics in susceptible families, it has been proposed that malignant hyperthermia may also involve cardiac muscle. To evaluate this, myocardial oxygen 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 oxygen consumption, lactate, potassium and catecholamine values, and acid-base balance. Ten genetically susceptible swine, five of which received propranolol, 40 μg/kg/min, continuously intravenously, were given halothane, 1 per cent, and succinylcholine, 3 mg/kg, to initiate malignant hyperthermia. Six normal swine, one 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 oxygen consumption increased from 7 to 34 ml O2/min/100 g heart. Swine given propranolol did not have increased myocardial oxygen consumption during malignant hyperthermia, but had myocardial oxygen consumption values similar to those of normal swine with or without propranolol. Also, during malignant hyperthermia, the myocardium did not release either lactate or potassium. The authors conclude that porcine malignani hyperthermia increases myocardial metabolism secondary to beta-adrenergic receptor stimulation due to increased release of catecholamines, and that it is unlikely that the myocardium is primarily involved in malignant hyperthermia.
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Gronert et al. (1978) studied Malignant hyperthermia (n=16). Propranolol vs. No propranolol was evaluated on Myocardial oxygen consumption. Propranolol prevented the increase in myocardial oxygen consumption during malignant hyperthermia in susceptible swine.
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