Pharmacology

1. 
   

   Insulin, a hormone secreted by the beta cells of the pancreas, promotes cellular uptake of glucose into skeletal and cardiac muscles and adipose tissue. Insulin shifts potassium intracellularly.

   
   
2. 
   

   The mechanism by which insulin-dextrose (hyperinsulinemia-euglycemia [HIE]) therapy improves inotropy and increases peripheral vascular resistance is not known. Calcium antagonists inhibit insulin secretion by blocking the L-type calcium channels of pancreatic islet cells and induce insulin resistance. Insulin may reverse the hyperglycemia, hypoinsulinemia, and acidosis commonly observed in calcium antagonist poisoning. In calcium antagonist and beta-adrenergic blocker overdose, myocardial metabolism shifts from free fatty acid to carbohydrate metabolism. Insulin stimulates myocardial metabolism and inhibits free fatty acid metabolism. Insulin may also improve glucose uptake by cardiac myocytes.

   
   
3. 
   

   Human regular insulin is biosynthetically prepared with recombinant DNA technology. The onset of action to decrease blood glucose for regular insulin is 30 minutes–1 hour, and the duration of action is 5–8 hours. The serum half-life of regular insulin is 4–5 minutes after IV administration.

Indications

1. 
   

   Hyperglycemia and diabetic ketoacidosis.

   
   
2. 
   

   Severe hyperkalemia (See Diagnosis of Poisoning).

   
   
3. 
   

   Administration with dextrose for hypotension induced by calcium antagonists (See Beta-Adrenergic Blockers) and beta-adrenergic blockers (See Arsine). Improved hemodynamics have been reported in case reports of patients with calcium antagonist toxicity and beta-adrenergic blocker overdose.

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