SUMMARY Using a pH-sensitive radiotelemetering device the effect of lactulose on luminal pH in the ileum, colon, and rectum has been compared with that of two other laxative agents.Lactulose produced marked acidification of proximal colonic contents but this effect was not consistently maintained into the distal colon. Sodium sulphate acidified distal rather than proximal colonic contents. However, for a similar degree of laxation it was not possible to produce a significantly more uniform reduction of pH along the length of the colon by combining these laxatives compared with lactulose alone. Magnesium sulphate had little effect upon luminal pH except in the rectum where a significant rise occurred.These results are discussed in relation to both normal colonic physiology and to their possible relevance to the treatment of chronic hepatic encephalopathy by colonic acidification.

I. The effect of increasing dietary protein content on the amount of faecal nitrogen was measured in six normal subjects and five subjects without functioning colons (three with ileostomy and two with ileo-rectal anastomosis).2. There was a significant increase in the amount of faecal N with increased dietary protein content in the subjects without functioning colons. 3.In normal subjects with intact colons, faecal N content was found to be lower than that in subjects without colons, and furthermore there was no significant variation with diet. 4.The source of the increase in faecal N with increased dietary protein content in subjects without functioning colons is discussed and the significance of these findings in relation to the efficiency of protein absorption is considered.The improvement in hepatic encephalopathy which follows purgation and enemas in the amount of dietary protein has an effect on the amounts of nitrogenous compounds entering the colonic lumen from the ileum. The extent of this process in man has never been measured and we have therefore determined the effect of varying dietary protein content on the amount of nitrogen entering the colon, as part of a study of the origin of gastrointestinal NH,. METHODS SubjectsThe six control subjects were either members of the medical staff of the hospital or patients with no evidence of small intestine or large intestine disease. Ileal N output was estimated in five other subjects, three with an ileostomy, one with an ileo-rectal anastomosis following colonic exclusion and one with an ileo-rectal anastomosis following colectomy, all of whom had undergone operation at least I year before this study and showed no evidence of recurrent disease, ileostomy dysfunction or obstruction at the ileo-rectal anastomosis. Informed consent was obtained from all subjects. DietsAll subjects were given a low (40 g/d)-and a high ( IOO g/d)-protein diet. The diet were isoenergetic (10.5 MJ/d), and the low-and high-protein diets provided (g/d) J. A. GIBSON, G. E. SLADEN AND A. M. DAWSON I976 N estimationsThe N content of paired, weighed portions of faecal homogenate was measured using a modified Kjeldahl digestion with a mercury catalyst (McKenzie & Wallace, 1954). From this value, the daily faecal N excretion was calculated for each subject for the low-and high-protein diets.Statistical analysis of the results was carried out using Student's t test. R E S U L T SIncreasing the amount of dietary protein, in all subjects, resulted in an increase in blood urea concentration (mean k SE) from 3.63 0.31 mmol/l with the low-protein diet to 5-98 f 0.27 mmol/l with the high-protein diet. This increase was highly significant (paired t test: t 7'925, P < 0.001).In control subjects neither faecal N excretion (g/d) nor faecal N concentration (g N/kg faeces) was increased significantly by increasing the amount of dietary protein (paired t test: t 2.489, 0.1 > P > 0.05; t 0.906, 0.5 > P > 0.4 for low-and highprotein diets respectively ( Table I)).Conversely in subjects with nonfunctio...

SUMMARY In iii'o rectal dialysis was used to study rectal mucosal release of immunoreactive prostaglandin E2-like material and its relation to disease activity, rectal electrical potential difference (PD), and treatment in 24 patients with ulcerative colitis. In untreated colitics in remission and in relapse, median values for apparent mucosal prostaglandin E2 (PGE2) release were increased three-fold (P <0.05) and 13-fold (P <0-002) respectively over that found in control subjects. In patients in remission during treatment with sulphasalazine and/or corticosteroids, median apparent PGE2 release was similar to that of controls, but in colitics in relapse, despite treatment, it was greatly increased (p < 0.002). Ulcerative colitis in relapse was associated with a significant reduction in rectal PD (p < 0.002); in patients with quiescent ulcerative colitis, a smaller reduction was found (p <0.05). In nine patients studied serially before and during treatment, there were associations between changes in disease activity assessed sigmoidoscopically, in PD and in apparent mucosal PGE2 release. Furthermore, rectal mucosal PGE2 release and PD were linearly correlated (p < 00 1). These findings indicate that mucosal PGE2 release is markedly enhanced in active ulcerative colitis, and they confirm the value of rectal PD as a guide to disease activity. In addition, they suggest that rectal dialysis may be a useful way of studying rectal prostaglandin metabolism in man.

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