Effects of glucose-insulin-potassium solution on free fatty acid metabolism in ischemic myocardium.

The accumulation of intermediates subsequent to impaired oxidation of free fatty acids has been suggested as a cause of cellular damage in ischemic myocardium. Many reviews have supported the theory that glucose-insulin-potassium (GIK) solution has a beneficial effect on the ischemic myocardium. We evaluated the effects of GIK solution on intermediates of free fatty acid metabolism in ischemic myocardium. The left coronary artery was occluded for 40 minutes in twelve dogs. In six dogs, 10 minutes before coronary artery occlusion, GIK solution (50 percent of glucose, 50 units/liter of regular insulin, 50 mEq/liter of potassium) was given at the rate of 0.1 ml/kg per minute until the time of excision of the heart. In the ischemic area, adenosine triphosphate (ATP) level in the GIK group (3.80 +/- 1.34 mumole/g) was significantly higher than that in the control group (2.04 +/- 0.68, p less than 0.05). The free carnitine level was significantly increased was GIK in both ischemic and nonischemic areas (p less than 0.05). In the control group, the long chain acyl coenzyme A (CoA) level in the ischemic area (23.0 +/- 7.0 nmole/g) was significantly higher than that in the nonischemic area (17.1 +/- 3.5, p, less than 0.05). On the other hand, GIK prevented the increase in the long chain acyl CoA in the ischemic area (17.8 +/- 5.6). This study suggests that GIK has a protective effect on ischemic myocardium, probably by preventing the accumulation of long chain acyl CoA by improving free fatty acid metabolism.