1982 Volume 46 Issue 7 Pages 657-662
Twenty-nine anesthetized mongrel dogs were subjected to characterize the effect of lidocaine in ischemic reperfused myocardium. The left anterior descending coronary artery was ligated for 40 min and reperfused for 15 min. Two mg/kg of lidocaine was administrated intravenously prior to the ligation and 2 mg/min (= 0.12 mg/kg/min) was infused continuously throughout the periods of coronary artery ligation and the reperfusion. Hemodynamic indices of left ventricular function were measured before ligation, 40 min after ligation and after 15 min of reperfusion, respectively. Transmural myocardial samples obtained from both the ischemic and non-ischemic regions after 15 min of reperfusion were divided into the subendocardial and subepicardial layers and used for measurements of adenosine triphosphate (ATP), creatine phosphate (CP) and water content. ATP in ischemic endocardium was 1.73±0.69μmole/g in the lidocaine-treated group and 1.36±0.41 in the non-treated group (p<0.05), and CP was 2.38±0.90 μmole/g and 1.59±0.95, respectively (p<0.01). Thus, high energy phosphate was at a significantly higher level in the lidocaine-treated group. Water content was significantly higher level in the lidocaine-treated group as compared with the non-treated group. Coronary blood flow and left ventricular functions were not significantly different between the two groups. These data suggest that lidocaine has a protective effect on ischemic reperfused myocardium and does not depress the left ventricular function in the commonly used doses.