Malignant hyperthermia phenotype - Hypotension induced by succinylcholine in susceptible swine

Background: Saccinylcholine causes immediate and severe arterial hypotensio n in swine with the malignant hyperthermia phenotype, The underlying mechan isms are unknown, Methods: Malignant hyperthermia-susceptible (MHS; n = 10) and normal swine (n = 5) were anesthetized with thiopental. The following were monitored: el ectrocardiogram; arterial blood pressure; pulmonary artery, central venous, and left and right ventricular pressure; cardiac output; end-tidal carbon dioxide; core temperature; peripheral-blood flows; and arterial blood gases . After a control period, 2 mg/kg succinylcholine was given intravenously, Three MHS animals received 1 mg/kg vecuronium and two MHS animals received 2.5 mg/kg dantrolene intravenously. The effects of succinylcholine on left and right ventricular pressure and contractility were analyzed In isolated hearts. The effects of 0.06 nM succinylcholine on isometric tension develop ment were recorded in isolated femoral artery rings. Results: Succinylcholine caused an early, severe decrease in blood pressure , cardiac output, left ventricular pressure, and left ventricular contracti lity in MHS swine but not in normal swine; no significant differences were found in heart rate, right ventricular parameters, systemic vascular resist ance, and preload (pulmonary diastolic pressure, central venous pressure). The succinylcholine-induced hypotension and associated effects were not pre vented by dantrolene, However, pretreatment with high-doss vecuronium preve nted not only the cardiovascular depression, but also MH. In addition, no p henotypic differences of succinylcholine on contractility or left ventricul ar pressure were observed in the isolated working hearts. Similary, succiny lcholine did not cause a significantly different relaxation in rings in eit her phenotype. Conclusion: Succinylcholine-induced hypotension occurred before muscle hype rmetabolism in MHS swine, Succinylcholine had no differential physiologic e ffects on either the isolated heart or on isolated arteries. This hypotensi on could not be prevented by dantrolene but was prevented by pretreatment w ith high-dose vecuronium. Thus, an indirect mechanism such as the release o f a cardiac depressant from skeletal muscle may have caused this hypotensiv e response.