Regional Myocardial Lidocaine Concentration Determines the Antidysrhythmic Effect in Dogs after Coronary Artery Occlusion

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Abstract
Ischemic ventricular dysrhythmias were produced in 40 of 47 anesthetized mongrel dogs by high ligation of the left anterior descending coronary artery. Dysrhythmias were treated with a single i.v. bolus of 20, 40, 80, or 120 mg of lidocaine (L) in order to determine the dose at which .apprx. 50% of animals had an antidysrhythmic response. Cardiac output and regional myocardial blood flow (RMBF) were measured by using radionuclide labeled microspheres. Lidocaine concentration ([L]) was measured from samples of arterial and venous blood and normal and ischemic myocardium. All dogs treated with 40, 80 or 120 mg of L had an antidysrhythmic effect. However, with 20 mg of L the dysrhythmia persisted in 12 and resolved in 14. With 20 mg of L, ischemic myocardial [L] was greater in dogs with an antidysrhythmic effect than in those with persistent dysrhythmias (1.14 .+-. 0.12 vs. 0.76 .+-. 0.04 .mu.g .cntdot. mg-1), but no difference was seen for arterial, venous, and normal myocardial [L]. Ischemic RMBF was higher in the dogs that had an antidysrhythmic effect than in those that did not, 9.8 .+-. 1.5 vs. 6.9 .+-. 1.3% of normal. With 20 mg of L, [L] in ischemic myocardium correlated well with ischemic RMBF. The antidysrhythmic response to L had a threshold at a tissue concentration of greater than or equal to 1.0 .mu.g .cntdot. g-1 (chi-square = 8.55, P < 0.005). For this model, the [L] in ischemic myocardium during acute ischemic correlates with the antidysrhythmic response to L, while the concentration in normal myocardium or blood does not.

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