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To determine the effect of hypoglycemia on myocardial ischemic injury following coronary artery occlusion epicardial electrograms were recorded 15 minutes after two 20-minute coronary artery occlusions in seven anesthetized dogs. The first occlusion was a control (blood glucose 85 plus or minus 5(sd) mg per cent). Before the second occlusion hypoglycemia was induced (blood glucose 40 plus or minus 5 mg per cent) by the intravenous administration of insulin (2 units/kg). The average ST-segment elevation in leads during control was 3.5 plus or minus 1.0 mV which rose to 6.1 plus or minus 1.4 mV during the second occlusion (P smaller than 0.05). The number of sites showing ST-segment elevation exceeding 2 mV increased from 7.6 plus or minus 1.6 during control to 10.6 plus or minus 1.4 (P smaller than 0.05) during the occlusion with hypoglycemia. In other dogs, a coronary artery was occluded for 24 hours. 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 plus or minus 6.0 IU/mg protein. Six additional dogs received insulin following the 15 minute epicardial map and blood sugar was maintained at a level of 46 plus or minus 6 mg per cent for the 24 hours. These dogs showed more myocardial necrosis than predicted by the ST-segment elevation prior to insulin administration. Forty-six percent 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.

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