The effect of hypoglycemia on myocardial ischemic injury during acute experimental coronary artery occlusion

Abstract

To determine the effect of hypoglycemia on myocardial ischemic injury following coronary artery occlusion epicardial electrograms were recorded 15 min after two 20 min coronary artery occlusions in 7 anesthetized dogs. The first occlusion was a control (blood glucose 85 ± 5(SD) mg%). Before the second occlusion hypoglycemia was induced (blood glucose 40 ± 5 mg%) by the intravenous administration of insulin (2 units/kg). The average ST segment elevation in leads during control was 3.5 ± 1.0 mV which rose to 6.1 ± 1.4 mV during the second occlusion (P < 0.05). The number of sites showing ST segment elevation exceeding 2 mV increased from 7.6 ± 1.6 during control to 10.6 ± 1.4 (P < 0.05) during the occlusion with hypoglycemia. In other dogs, a coronary artery was occluded for 24 hr. Epicardial ST segment elevations were compared to creatine phosphokinase (CPK) activity and histological appearance from the same sites. CPK activity in sites with normal ST segments (0-2 mV) was 33.1 ± 6.0 IU/mg protein. 6 additional dogs received insulin following the 15 min epicardial map and blood sugar was maintained at a level of 46 ± 6 mg% for the 24 hr. These dogs showed more myocardial necrosis than predicted by the ST segment elevation prior to insulin administration. 46% of sites, which in control dogs would have been expected to have normal CPK and histological appearance, showed depressed CPK activity and histological evidence of early myocardial necrosis. Thus, hypoglycemia increases myocardial damage, as reflected by enzymatic and histological analyses.