Buffington C W
Department of Anesthesiology, University of Washington, Seattle.
Anesthesiology. 1989 Feb;70(2):280-7. doi: 10.1097/00000542-198902000-00017.
Direct myocardial depression plays a role in the cardiovascular toxicity of local anesthetic agents, but this role is obscured by concomitant cardiac, systemic, and CNS events: seizures, hypoxia, acidosis, sympathetic activation, bradycardia, and A-V heart block. Direct injection of small bolus doses of lidocaine and bupivacaine into a branch of the left coronary artery was used to minimize these systemic effects. Regional contraction in the zone supplied by the coronary artery was measured with a sonomicrometer. Both agents caused a dose-dependent reduction in the extent of systolic contraction, and a 4.9:1 (lidocaine:bupivacaine) dose ratio produced a 50% depression of contraction. The duration of depression, taken as the time for 95% recovery of systolic contraction, was about 25% (P less than 0.05) longer with bupivacaine for an equal degree of depression. Coronary blood flow was reduced modestly by both agents. These results suggest that differences in the magnitude or duration of direct myocardial depression cannot explain the clinical perception that the cardiovascular toxicity of bupivacaine is greater than that of lidocaine.
直接心肌抑制在局部麻醉药的心血管毒性中起作用,但这种作用被同时发生的心脏、全身和中枢神经系统事件所掩盖:癫痫发作、缺氧、酸中毒、交感神经激活、心动过缓和房室传导阻滞。将小剂量推注利多卡因和布比卡因直接注入左冠状动脉分支,以尽量减少这些全身效应。用超声测距仪测量冠状动脉供血区域的局部收缩。两种药物均导致收缩期收缩程度呈剂量依赖性降低,4.9:1(利多卡因:布比卡因)的剂量比可使收缩降低50%。在同等程度的抑制下,布比卡因导致的抑制持续时间(定义为收缩期收缩恢复95%的时间)比利多卡因长约25%(P<0.05)。两种药物均使冠状动脉血流量略有减少。这些结果表明,直接心肌抑制的程度或持续时间的差异无法解释临床上认为布比卡因的心血管毒性大于利多卡因的观点。