Endogenous corticosteroids and insulin in acute inflammation

Carrageenin-induced inflammatory responses in the hindpaws of rats were quantitated by measuring: (1) alterations in volumes of the paws; and (2) alterations in concentration of dye, previously injected intravenously, which was recovered in perfusates from the paws. The inflammatory response in one paw was attenuated by previously inducing an inflammatory response in the contralateral paw. The effect was abolished by pretreatment with insulin. Indexes of adrenal activity were increased after the induction of the inflammatory response and they were not attenuated by pretreatment with insulin. Adrenal hyperactivity was characterized by increased serum corticosterone concentration, decreased adrenal ascorbic acid content, and reduced number of circulating eosinophils. It is concluded that inflammatory stimuli which lead to alterations in microvessels depend on a facilitatory effect of insulin. This effect is antagonized by glucocorticoids released in enhanced concentrations after the application of noxious stimuli. Therefore, endogenous insulin and glucocorticoids act as modulators of inflammatory responses.

Keywords

ascorbic acid, carrageenan, glucocorticoid, insulin, adrenal gland, animal experiment, animal model, biological model, blood and hemopoietic system, blood vessel permeability, controlled study, corticosterone blood level, edema, endocrine system, eosinophil, inflammation, intravenous drug administration, peripheral vascular system, rat, subcutaneous drug administration, Adrenal Cortex, Animal, Ascorbic Acid, Capillary Permeability, Carrageenan, Corticosterone, Edema, Eosinophils, Hindlimb, Inflammation, Insulin, Leukocyte Count, Male, Rats, Rats, Inbred Strains, Support, Non-U.S. Gov't