RESUMO
The effect of atropine on meal-stimulated gastric inhibitory polypeptide (GIP) and gastrin release was studied in 5 purebred foxhounds and compared with control studies done in the same animals given a meal without atropine, peak incremental serum gastrin occurred between 5 and 15 min after the meal whereas the greatest increment in serum GIP occurred 60 min postcibal. Atropine had no effect on basal concentrations of gastrin or GIP. However, when atropine was given before feeding serum gastrin concentrations from 75 to 120 min postcibal were significantly higher (P less than 0.04) than after the meal alone. The normal meal-stimulated rise in serum GIP was almost completely inhibited by atropine. We conclude that: 1) the rise in serum gastrin adter a meal preceeds the rise in serum GIP; 2) atropine potentiates the late gastrin response while suppressing the increase in serum GIP after a meal; and 3) the mechanism by which atropine potentiates gastrin release may be related to its suppressive effects on intestinal inhibitors of gastrin secretion, such as GIP.
Assuntos
Atropina/farmacologia , Ingestão de Alimentos , Polipeptídeo Inibidor Gástrico/metabolismo , Gastrinas/metabolismo , Hormônios Gastrointestinais/metabolismo , Animais , Cães , CinéticaRESUMO
Of 42 critically ill patients with toxic megacolon, 31 required emergency surgery, and 11 were treated without operation. Of the 11 patients treated by medical measures alone, there were two deaths (18%): one early, secondary to undiagnosed colonic perforation, and one late death from recurrent ulcerative colitis. Nine of ten survivors (90%) experienced continued morbidity, and five (50%) required subsequent elective surgery. Thirty-one patients required emergency operation for failure of medical treatment (19), colonic perforation (ten), and uncontrolled hemorrhage (two). Early and late morbidity was 74% (two-thirds occurring after subtotal colectomy and ileostomy). Surgical mortality was 19% (8% over the last ten years).