1. A technique is described for the removal of subcellular contaminants from intact rat intestinal brush borders, and for the subsequent separation of a microvillus membrane fraction from a fibrillar residue. 2. Increments in invertase activity, microscopic homogeneity and low nucleic acid content indicate that the microvillus plasma membrane has been extensively purified. Multiple membrane preparations have been shown to be highly reproducible with respect to their invertase specific activity, cholesterol content and phospholipid content. Alkaline phosphatase, leucine aminopeptidase, Mg(2+)- and Ca(2+)-dependent adenosine triphosphatase and seven separate disaccharidases were shown to be predominantly confined to the membrane fraction. 3. The fibrillar fraction has been shown to contain approximately 30% of the total protein of purified brush borders, plus most of the residual nucleic acid contaminant. No evidence was found for the localization of any specific enzyme in this fraction.

Previously, we demonstrated that the hydrophobic surfactant Pluronic L-81 (L-81) inhibits the intestinal formation and transport of chylomicrons (CM) but not of very low-density lipoprotein-sized (VLDL) particles. The present study was undertaken to determine whether infusion of egg lecithin results mainly in secretion of VLDL by the small intestine and whether L-81 has any effect on their formation and secretion. Intestinal fistula rats were infused intraduodenally at a rate of 3 ml/h with a lipid emulsion containing 20 mM egg lecithin and 19 mM sodium taurocholate for 8 h. This was then followed by another 8 h of infusion of a similar lipid emulsion but with 0.5 mg/h of L-81 added. Lymphatic lipid output was measured, and lymph lipoproteins were sized by use of electron microscopy. Whether L-81 was present or not, no significant difference was detected in the lymphatic triglyceride, phospholipid, or cholesterol outputs. Based on agarose gel electrophoresis, sizing of intestinal lymph lipoproteins, and also the determination of lipid in the intestinal lymph CM and VLDL as separated by ultracentrifugation, VLDL were the major lipoproteins present in lymph during the infusion of egg lecithin. Thus, intraduodenal infusion of egg lecithin in the rat results mainly in the transport of VLDL and is not affected by the administration of L-81. The results suggest that CM and VLDL are assembled separately by the enterocytes and indicate the usefulness of L-81 in further investigating the pathways and regulation of intestinal lipoprotein synthesis, assembly, and secretion.

Three hundred seventy patients with recently healed duodenal ulcer entered into a one-year, double-blind, randomized multicenter trial comparing placebo with three different dose schedules of cimetidine (200 mg twice a day, 300 mg twice a day, and 400 mg at bedtime) for the prevention of recurrent duodenal ulcer. By the end of one year, the cumulative symptomatic recurrence rate as demonstrated by endoscopy was similar for the patients receiving the three dosages of cimetidine (19 per cent, 15 per cent, and 13 per cent, respectively; not significant), whereas the placebo-treated group had a 34.7 per cent symptomatic recurrence rate (P less than 0.01 as compared with each cimetidine group). Cigarette smoking was found to be an important variable; among the placebo recipients ulcer recurrence was significantly more likely in smokers (72 per cent) than in nonsmokers (21 per cent, P less than 0.001). The frequency of ulcer recurrence in smokers was significantly reduced by treatment with cimetidine (from 72 per cent to 34 per cent, P less than 0.). Smokers who received cimetidine were at least as likely to have a recurrence as were nonsmokers who received placebo (34 per cent vs. 21 per cent, not significant). Thus, smoking appears to be a major factor in recurrence of duodenal ulcer, and in smokers, giving up smoking may be more important in the prevention of ulcer recurrences than administration of cimetidine.

Treatment of rats with puromycin and acetoxycycloheximide results in a defect in intestinal lipid transport. Under these conditions rats given corn oil accumulate triglyceride within the intestinal cells and fail to develop the normal postprandial hyperlipemia. The observed interference in lipid transport appears to be a consequence of impaired chylomicron formation.