Lidocaine-induced reduction in size of experimental myocardial infarction.

In anesthetized open chest dogs, the effects of therapeutic doses of lidocaine on myocardial cell respiration, creatine kinase depletion, left ventricular stroke work and cardiac necrosis were assessed. The dogs were subjected to 40 minutes of occlusion of the left anterior descending coronary artery, followed by 5 hours of reperfusion. Group I (12 dogs) had infusion of saline solution; group II (8 dogs) had infusion of 0.2 mg/kg per min of lidocaine (serum level 16.8 +/- 1.4 microgram/ml); group III (5 dogs) had infusion of 0.04 mg/kg per min or lidocaine (serum level 3.6 micrograms/ml). Ischemic regional myocardial blood flow (measured by 9 micrometer spheres of strontium-85) was 6.34 +/- 1.62 ml/100 mg per min in group I, 1.48 +/- 0.59 in group II (p < 0.05) and 1.32 +/- 0.50 in group III (p < 0.05). Oxygen consumed during conversion of adenosine diphosphate to adenosine triphosphate in mitochondria from control and lidocaine-treated ischemic tissue was depressed (p < 0.05) and correlated (r = 0.63) with creatine kinase depletion. Left ventricular stroke work was not significantly different among the three groups. Infarct size (in percent of left ventricular weight) was 12.6 +/- 2.0 for group I, 4.8 +/- 1.2 for group II (p < 0.01) and 4.8 +/- 2.5 for group III (p < 0.05). The data suggest that the reduction of myocardial infarct size by lidocaine was not dependent on enhanced myocardial blood flow and was independent of left ventricular stroke work.