Is insulin an endogenous cardioprotector?
Stress hyperglycemia and diabetes mellitus with myocardial infarction are associated with increased risk for in-hospital mortality, congestive heart failure, or cardiogenic shock. Hyperglycemia triggers free radical generation and suppresses endothelial nitric oxide generation, and thus initiates and perpetuates inflammation. Conversely, insulin suppresses production of tumor necrosis factor-alpha and free radicals, enhances endothelial nitric oxide generation, and improves myocardial function. It is proposed that the balance between insulin and plasma glucose levels is critical to recovery and/or complications that occur following acute myocardial infarction and in the critically ill. Adequate attention should be given to maintaining euglycemia (plasma glucose <or= 110 mg/dl) in order to reduce infarct size and improve cardiac function while using a glucose-insulin-potassium cocktail.
Das
Undurti N
UN
EFA Sciences LLC, Norwood, Massachusetts, USA. undurti@hotmail.com
D000328:Adult; D000818:Animals; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D006943:Hyperglycemia / Q000150:complications*; D007328:Insulin / Q000502:physiology* / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D051381:Rats; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D001786:Blood Glucose; D007328:Insulin; D014409:Tumor Necrosis Factor-alpha