Huang Y F, Upton R N, Runciman W B
Department of Anaesthesia and Intensive Care, Royal Adelaide Hospital, University of Adelaide, Australia.
Br J Anaesth. 1993 May;70(5):556-61. doi: 10.1093/bja/70.5.556.
We have studied relationships between the time-courses of lignocaine concentrations in arterial and coronary sinus blood and myocardial tissue, and negative inotropic effects on the myocardium, after i.v. bolus administration of 50-, 75- or 100-mg doses of lignocaine to conscious, chronically instrumented sheep. Peak arterial and coronary sinus blood lignocaine concentrations occurred 26-38 s before and 29-78 s after the maximum decreases in myocardial contractility, respectively. Peak myocardial concentrations occurred simultaneously with the maximum decreases in myocardial contractility, except for the 100-mg doses. Anti-clockwise hysteresis occurred only between arterial blood lignocaine concentrations and the negative inotropic effect. It was concluded that, after short-term i.v. administration, only the myocardial concentrations of lignocaine were in pseudoequilibrium with the negative inotropic effects of the lignocaine on the myocardium.
我们研究了在对有意识的、长期植入仪器的绵羊静脉注射50毫克、75毫克或100毫克剂量的利多卡因后,动脉血和冠状窦血中利多卡因浓度的时程与心肌组织中利多卡因浓度的时程之间的关系,以及利多卡因对心肌的负性肌力作用。动脉血和冠状窦血中利多卡因浓度峰值分别在心肌收缩力最大下降之前26 - 38秒和之后29 - 78秒出现。除了100毫克剂量外,心肌浓度峰值与心肌收缩力最大下降同时出现。逆时针滞后现象仅出现在动脉血利多卡因浓度与负性肌力作用之间。得出的结论是,短期静脉给药后,只有心肌中的利多卡因浓度与利多卡因对心肌的负性肌力作用处于假平衡状态。