Improvement of cardiac preservation by preoperative high insulin supply

Therapeutic administration of high doses of insulin achieves a shifting of metabolism to glycogenesis and glycolysis. The result is an accumulation of the myocardial glycogen stores and an improvement of glucose utilization as well. If on that basis an increased anaerobic provision of adenosine triphosphate will be maintained in the myocardium during ischemia, the myocardial cell viability during aortic cross-clamping will be saved as well. Thus a preventive insulin supply will preserve the heart from ischemic damage. Twenty patients undergoing mitral valve replacement were investigated in two randomized groups. One group received insulin (1 U/kg/hr) together with a 33% glucose infusion (0.5 gm/kg/h) and potassium (0.25 mEq/kg/hr) from the onset of anesthesia until aortic cross-clamping. The control group received Ringer's lactate at the same infusion rate. After an average ischemic time of 26 minutes, an excised papillary muscle tip was immediately plunged into liquid nitrogen and the content of adenosine triphosphate, adenosine diphosphate, and creatine phosphate was determined. The adenosine triphosphate/diphosphate quotient and the energy charge potential were calculated. The mean adenosine triphosphate content in the insulin group was 7.43 mumol/gm wet weight and was significantly (p less than 0.01) higher than that of the control group (4.28 mumol/gm). The mean ADP content was 1.43 mumol/gm in the insulin group versus 1.81 mumol/gm in the control group. The mean creatine phosphate content was again significantly (p less than 0.05) higher in the insulin group (6.70 mumol/gm) than in the control group (5.30 mumol/gm). Also, the mean adenosine triphosphate/diphosphate quotient (insulin group, 5.19; control group, 2.36) and the mean energy charge potential (insulin group, 0.919; control group, 0.851) were significantly (p less than 0.01) higher in the insulin group. It is concluded that the preventive application of high doses of insulin leads to an augmented myocardial adenosine triphosphate provision and a maintained cellular energy charge during coronary ischemia. As a result, ischemic tolerance is enhanced and myocardial protection is improved.