Sigg D C, Iaizzo P A
Departments of Anesthesiology and Physiology, University of Minnesota, Minneapolis, Minnesota 55455, USA.
Anesthesiology. 2000 Jun;92(6):1777-88. doi: 10.1097/00000542-200006000-00038.
Succinylcholine causes immediate and severe arterial hypotension in swine with the malignant hyperthermia phenotype. The underlying mechanisms are unknown.
Malignant hyperthermia-susceptible (MHS; n = 10) and normal swine (n = 5) were anesthetized with thiopental. The following were monitored: electrocardiogram; 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 mm succinylcholine on isometric tension development were recorded in isolated femoral artery rings.
Succinylcholine caused an early, severe decrease in blood pressure, cardiac output, left ventricular pressure, and left ventricular contractility in MHS swine but not in normal swine; no significant differences were found in heart rate, right ventricular parameters, systemic vascular resistance, and preload (pulmonary diastolic pressure, central venous pressure). The succinylcholine-induced hypotension and associated effects were not prevented by dantrolene. However, pretreatment with high-dose vecuronium prevented not only the cardiovascular depression, but also MH. In addition, no phenotypic differences of succinylcholine on contractility or left ventricular pressure were observed in the isolated working hearts. Similary, succinylcholine did not cause a significantly different relaxation in rings in either phenotype.
Succinylcholine-induced hypotension occurred before muscle hypermetabolism in MHS swine. Succinylcholine had no differential physiologic effects on either the isolated heart or on isolated arteries. This hypotension could not be prevented by dantrolene but was prevented by pretreatment with high-dose vecuronium. Thus, an indirect mechanism such as the release of a cardiac depressant from skeletal muscle may have caused this hypotensive response.
琥珀酰胆碱可使具有恶性高热表型的猪立即出现严重动脉低血压。其潜在机制尚不清楚。
将恶性高热易感猪（MHS；n = 10）和正常猪（n = 5）用硫喷妥钠麻醉。监测以下指标：心电图；动脉血压；肺动脉、中心静脉以及左右心室压力；心输出量；呼气末二氧化碳；核心体温；外周血流量；以及动脉血气。在对照期后，静脉注射2mg/kg琥珀酰胆碱。3只MHS动物静脉注射1mg/kg维库溴铵，2只MHS动物静脉注射2.5mg/kg丹曲林。分析琥珀酰胆碱对离体心脏左右心室压力及收缩性的影响。记录0.06mm琥珀酰胆碱对离体股动脉环等长张力发展的影响。
琥珀酰胆碱使MHS猪的血压、心输出量、左心室压力和左心室收缩性早期出现严重下降，但正常猪未出现；心率、右心室参数、全身血管阻力和前负荷（肺舒张压、中心静脉压）无显著差异。丹曲林不能预防琥珀酰胆碱诱导的低血压及相关效应。然而，高剂量维库溴铵预处理不仅可预防心血管抑制，还可预防恶性高热。此外，在离体工作心脏中未观察到琥珀酰胆碱对收缩性或左心室压力的表型差异。同样，琥珀酰胆碱在两种表型的动脉环中引起的舒张无显著差异。
在MHS猪中，琥珀酰胆碱诱导的低血压发生在肌肉代谢亢进之前。琥珀酰胆碱对离体心脏或离体动脉无差异生理效应。这种低血压不能被丹曲林预防，但可被高剂量维库溴铵预处理预防。因此，骨骼肌释放心脏抑制因子等间接机制可能导致了这种低血压反应。
