AIM:
Lidocaine inhibits depolarization by blocking sodium and calcium influx and potassium release, abolishing the action potentials of cells in the Hiss-Purkinje system and myocit cells. As it can directly influence cardiac electric and mechanical activities, this study evaluated the efficacy of lidocaine in providing myocardial protection during normothermic blood cardioplegia.
METHODS:
Twenty-six dogs were randomly assigned to groups based on the cardioplegic induction solution they were to receive. Group I dogs (n=10) received a solution consisting of lidocaine (5 mg/kg), KCL (41.6 mEq/L) and 180 ml of normothermic blood. Group II dogs (n=10) received the same solution, except for the lidocaine and group III dogs (n=6) received only normothermic blood. In addition, 120 ml of normothermic blood was reinfused every 20 min. All dogs underwent cardiopulmonary bypass, 2 hours of global myocardial ischemia and 3 hours of reperfusion. Statistical differences were determined with the chi squared test, the two-way analysis of variance and Bonferroni’s test.
RESULTS:
There were no deaths in group I. The survival rate in group II was 60%, and no dogs in group III survived (p=0.025). No difference in lactate liberation or left ventricular function (i.e., cardiac outflow and ejection fraction) was observed between groups. However, animals in group I demonstrated less enzymatic releases (troponin I, p=0.049 and CK, p=0.026) and less mitochondrial ultrastructural changes (p=0.022).
CONCLUSIONS:
Lidocaine offers myocardium additional protection against ischemia during cardiopulmonary bypass.
