Evaluating the effects of rifampin in the prevention of neurogenic symptoms and cardiac arrhythmias caused by the systemic toxicity of lidocaine in rats

Lidocaine toxicity is caused by unintended intravascular injection or overdose. Lidocaine is metabolized in the liver by the CYP۳A۴ isoenzyme. The objective was to investigate if the administration of rifampin could accelerate animal recovery and reduce the symptoms of lidocaine toxicity by induction of the CYP۳A۴. Thirty-six male rats were divided into control and treatment groups, each containing three subgroups. The treatment group received oral rifampin suspension daily for ۱ week. In all rats, ۲.۰۰% lidocaine was injected intravenously. The first subgroup was monitored for neurological symptoms. In the second subgroup, data were recorded after the electrode was placed in the right hippocampus. Electrocardiograms were taken from the third subgroup. CYP۳A۴ was measured using an ELISA kit. Neurological recovery was seen after ۲۲ and ۱۵ min in the control and treatment groups, respectively. Rifampin also caused a significant reduction in amplitude and number of field action potentials compared to the control group. Numerous cardiac arrhythmias were observed in the control group. The mean level of CYP۳A۴ in the treatment group was significantly higher than in the control group. In conclusion, oral rifampin could increase the synthesis of CYP۳A۴, therefore, the animal recovery from lidocaine toxicity was accelerated.

Keywords:

Anesthesia , Arrhythmia , Enzyme induction , Lidocaine toxicity , Rifampin