16-16-dimethylprostaglandin-e2 and Intestinal-Obstruction

Intestinal obstruction inhibits amino acid absorption. The inhibition, being dependent on the pathological changes of the absorptive epithelium, was considered as an index of injury and measured after varying periods of obstruction and after pretreatment with clindamycin, indomethacin, 16,16-dimethyl-PGE2 or arachidonic acid. A reduction in amino acid uptake was apparent after 2h of obstruction and was increasingly evident after 4, 6 and 18 h. During the late phase (after 6 h), inhibition was partly prevented by pretreatment with clindamycin, but the antibiotic was ineffective during the early phase (within the first 2 h). Bacterial colony counts of luminal contents of rats obstructed for 2 h, were not different from counts obtained in controls, but significantly lower than counts in rats that have been obstructed for 6 h. Pretreatment of rats with 16,16-dimethyl-PGE2 or with arachidonic acid prevented the early inhibitory effects of the obstruction. The findings suggest that the early inhibition in amino acid uptake may be related to metabolic changes that are correctable by the administration of 16,16-dimethyl-PGE2 or of arachidonic acid. The inhibition, during the late phase, is mainly related to an overgrowth of the enteric bacteria.

Topics: 16,16-Dimethylprostaglandin E2; Alanine; Animals; Arachidonic Acid; Arachidonic Acids; Clindamycin; Ileum; In Vitro Techniques; Indomethacin; Intestinal Absorption; Intestinal Obstruction; Inulin; Male; Prostaglandin Antagonists; Prostaglandins; Rats; Rats, Inbred Strains

Topics: 16,16-Dimethylprostaglandin E2; Animals; Atropine; Carbachol; Disease Models, Animal; Drug Interactions; Gastric Emptying; Gastrointestinal Motility; Guinea Pigs; Hydroxydopamines; Intestinal Obstruction; Male; Prostaglandins E, Synthetic; Rats; Sympathetic Nervous System

The prostaglandins PGF2 alpha, PGE2 and 16,16-dimethyl PGE2, when administered intravenously, orally, subcutaneously or intraduodenally to laparotomized rats, decreased gastric emptying, small intestinal transit and colonic transit as compared to unoperated controls. All three prostaglandins increased colonic transit above that found with unoperated controls. This activity was independent of small intestinal fluid accumulation (i.e., enteropooling) since ligating the ileal-cecal junction had no effect on colonic transit. Small intestinal transit was increased, but not normalized, by PGE2 and 16,16-dimethyl PGE2. 16,16-Dimethyl PGE2 completely restored gastric emptying when given intravenously to laparotomized rats of doses greater than 5.0 microgram/kg. This effect on gastric emptying lasted approximately 4 hrs. Thus, 16,16-dimethyl PGE2, when given intravenously, normalized gastric emptying, significantly increased small intestinal transit, and made the colon hypermotile. Prostaglandins may be beneficial in the treatment of postoperative ileus and other conditions of sluggish gastrointestinal propulsion.

Topics: 16,16-Dimethylprostaglandin E2; Animals; Colon; Gastric Emptying; Gastrointestinal Motility; Intestinal Obstruction; Intestine, Small; Male; Prostaglandins E; Prostaglandins F; Rats; Time Factors