The Effect of Clonidine Pretreatment on Bupivacaine-induced Cardiac Toxicity in Rabbit.
- Author:
Eun Ju LEE
1
;
Jin Young CHON
;
Yong Woo CHOI
;
Se Ho MOON
Author Information
1. Department of Anesthesiology, College of Medicine, Catholic University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Anesthetics;
local;
bupivacaine;
Complication;
cardiac toxicity;
Sympathetic nervous system;
pharmacology;
clonidine
- MeSH:
Anesthesia, Conduction;
Anesthetics;
Arterial Pressure;
Bupivacaine;
Cardiac Electrophysiology;
Catheters;
Clonidine*;
Electrocardiography;
Heart Arrest;
Heart Rate;
Hemodynamics;
Hypotension;
Infusions, Intravenous;
Ketamine;
Pharmacology;
Plasma;
Rabbits;
Sympathetic Nervous System;
Tracheostomy;
Ventilation;
Xylazine
- From:The Korean Journal of Critical Care Medicine
1998;13(2):205-211
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGOUND: Bupivacaine, an amide type local anesthetic, is frequently used for regional anesthesia. Bupivacaine overdose induces cardiac toxicity and directly depresses both cardiac electrophysiology and hemodynamic status. Clonidine, an imidazolin alpha-2-adrenoreceptor agonist, given prophylactically may delay the toxic manifestation of bupivacaine overdose and does not accentuate the subsequent hypotension. We studied the effect of clonidine pretreatment on bupivacaine induced cardiac toxicity. METHODS: Fourteen rabbits (seven in each group) were anesthetized with ketamine and rompun, and tracheostomy was performed. Spontaneous ventilation with room air was continued throughout the experiment. Electrocardiogram, heart rate, and invasive arterial blood pressure were continuously recorded. Clonidine 5 microgram/kg (clonidine group) or saline (control group) was injected intravenously in randomized fashion. After 15 minutes, an intravenous infusion of bupivacaine was started at 0.3 mg/kg/min. The time of occurrence of the bupivacaine-induced toxic events: first dysrhythmia, 25% and 50% reduction in basal heart rate and mean arterial pressure, and asystole were recorded. At 5, 10, 15, and 20 minutes after bupivacaine infusion, 2 ml of whole blood were withdrawn via femoral arterial catheter for determination of bupivacaine concentration. RESULTS: The threshold time at the first dysrhythmia was significantly greater in the clonidine group (27.2+/-4.5 min) than control group (19.9+/-1.2 min). The threshold times at the 25 and 50% reduction in basal heart rate were significantly greater in the clonidine group (23.7+/-5.8 min, 33.2+/-5.1 min) than control group (16.6+/-2.9 min, 22.9+/-2.8 min) and in basal mean arterial pressure were significantly greater in the clonidine group (15.6+/-2.6 min, 25.3+/-3.7 min) than control group (9.7+/-2.7 min, 16.3+/-5.8 min). The threshold time at the asystole was significantly greater in the clonidine group (38.2+/-7.7 min) than control group (28.7+/-3.4 min). At 5, 10, 15, and 20 minutes after bupivacaine infusion, there was no significant difference in the plasma bupivacaine concentration between two groups. CONCLUSION: This study demonstrates that clonidine pretreatment delays the cardiac toxic manifestations of bupivacaine overdose. And plasma bupivacaine concentration was not influenced by clonidine pretreatment.
