Mechanism of hyperglycemia induced by extensive wounds and generalized surgical infection.
Significant differences were revealed in the mechanism of hyperglycemia in extensive wounds and generalized surgical infection. Hyperglycemia in extensive burn injuries is caused by the inhibition of insulin formation, decreased insulin binding to cellular receptors, which leads to decreased sensitivity of tissues to insulin. Hyperglycemia developing in generalized infection is a result of insufficient blood insulin levels consequent to inhibition of its secretion (while insulin biosynthesis is elevated) under the effects of hyperproduction of prostaglandins, and is also mediated by defects in insulin-receptor interaction. Correction of carbohydrate metabolism disorders in these surgical pathologies in spite of the different pathogenetic mechanisms might be achieved by exogenous insulin administration, and also by insulin administration together with indomethacin, a nonsteroid anti-inflammatory agent, inhibiting prostaglandin production.
Morenkova
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D000818:Animals; D005947:Glucose / Q000378:metabolism; D006943:Hyperglycemia / Q000209:etiology*; D007213:Indomethacin / Q000494:pharmacology; D007328:Insulin / Q000096:biosynthesis / Q000097:blood; D007457:Iodine Radioisotopes; D008099:Liver / Q000378:metabolism; D008214:Lymphocytes / Q000378:metabolism; D009132:Muscles / Q000378:metabolism; D011453:Prostaglandins / Q000378:metabolism; D051381:Rats; D011972:Receptor, Insulin / Q000378:metabolism; D013530:Surgical Wound Infection / Q000097:blood / Q000150:complications*; D014947:Wounds and Injuries / Q000097:blood / Q000150:complications*
D007328:Insulin; D007457:Iodine Radioisotopes; D011453:Prostaglandins; D011972:Receptor, Insulin; D005947:Glucose; D007213:Indomethacin