The pharmacological modulation of angiogenesis in chronic granulomatous inflammation.

摘要: Angiogenesis is required for the progression of chronic inflammation, and agents that alter it can affect development inflammation consequent tissue destruction. However, in vivo quantification neovascularization its modulation by angiostatic angiogenic difficult. Studies have relied on reported effects drugs embryonic tumor vasculature to infer angiomodulatory actions. We characterized a vascular casting method incorporates carmine gelatin. Vascularity expressed as micrograms dye/mg dry (vascularity index, V.I.) was studied murine granulomatous air pouch. Carmine retained within gelatin, content increased before tissue, resulting V.I. peak at 5 days, regression second over 14 28 days. The prostaglandin synthesis, plasma exudation vasomotor tone showed remained unaffected, unlike Evans blue, illustrating independence from acute inflammatory processes such exudation. stimulus p.o. heparin V.I., whereas sub-anti-inflammatory dose cortisone with 1000 U reduced it. Higher doses overcame this. potent steroid tetrahydrocortisol significantly absence heparin. Cortisone exhibited topical administration hyaluronan. Dexamethasone inhibited increase These observations indicated differential anti-inflammatory activity. pharmacological angiogenesis therefore be quantified.