RESUMO
1. Evidence is presented for the occurrence of type 1 prostaglandin 15-hidroxydehydrogenase in human rectal mucosa. No evidence of the presence of type 2 dnzyme was found. 2. A 15-keto-prostaglandin reductase, responsible for the breakdown of 13, 14-dihydro 15-keto prostaglandins to 13, 14-dihydro prostaglandins, was also present in human rectal mucosa. 3. Ulcerative colitis patients catabolized prostaglandins to the same extent as the control group. PGE was catabolized significantly better than PGF2 alfa. 4. 5-Aminosalicylic acid and sulphapyridine did not affect prostaglandin catabolism. Sulphasalazine, methilsulphasalazine, indomethacin, flurbiprofen, disodium cromoglycate, sodium salicylate and carbenoxolone sodium inhibited prostaglandin catabolism to the same extent in both groups.Salicylazosulphadimidine was a more potent inhibitor of PGE1 catabolism than of PGF2alfa. 5. The increased prostaglandin synthesis reported for ulcerative colitis patients was not paralleled by increased catabolism, a fact possibly contributing to the accumulation of such compounds in the diseased state
Assuntos
Adulto , Pessoa de Meia-Idade , Humanos , Masculino , Feminino , Ácidos Aminossalicílicos/farmacologia , Colite Ulcerativa/metabolismo , Prostaglandinas E/metabolismo , Prostaglandinas F/metabolismo , Sulfassalazina/farmacologia , Ácidos Aminossalicílicos/uso terapêutico , Colite Ulcerativa/tratamento farmacológico , Mucosa Intestinal/patologia , NADP/metabolismo , Sulfassalazina/uso terapêuticoRESUMO
Las prostaglandinas (PG) E-2 y F-2 alfa tienen variadas acciones fisiologicas y farmacologicas. El presente trabajo es una revision bibliografica de estas acciones, profundizando en los efectos uterinos, farmacocinetica, las indicaciones, precauciones y contraindicaciones en su uso