Distribution and further studies on the activity of prostaglandin E in chronic granulomatous inflammation.
Pre-formed granulomata, induced by cannulated, carrageenin-soaked, subdermal sponge implants, were used to further analyse the effects of exogenous PGE and the involvement of endogenous PGE in this model of chronic inflammatory tissue changes in rats. Experiments with 14C-PGE2 indicated that administration of PGE into the sponge creates a kinetic situation likely to imitate, but superimposed upon, the continuous discharge of endogenous PGE in the granuloma. The granuloma-reducing, anti-flammatory effect of PGE can be mimicked by dibutyryl cyclic-AMP, phosphodiesterase inhibitors and indomethacin. Most probably these compounds, in common with PGE, exert their anti-granuloma action through elevation of intracellular cyclic-AMP (in macrophages and/or fibroblasts). The anti-granuloma action is not necessarily associated with a reduction in the endogenous PGE-level and vice versa. The involvement of endogenous PGE in the tissue events of granulomatous inflammation is conjectural as yet.
D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D002250:Carbon Radioisotopes; D002351:Carrageenan; D004195:Disease Models, Animal; D006105:Granulomatous Disease, Chronic / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D008797:Metyrapone / Q000494:pharmacology; D011458:Prostaglandins E / Q000378:metabolism* / Q000494:pharmacology; D051381:Rats
D002250:Carbon Radioisotopes; D011458:Prostaglandins E; D003994:Bucladesine; D002351:Carrageenan; D008797:Metyrapone