Biomedical subjects

D R Saunders

Publications and source records attributed to D R Saunders.

At least 55 records · Page 3Linked to original sources

PubMed1977

Human rectal mucosa: proctoscopic and morphological changes caused by laxatives.

To determine whether laxatives alter the proctoscopic and morphological appearances of the human rectum, 10 normal subjects were studied prospectively, and the following manipulations were assessed in a randomized, blinded manner: no treatment; oral mannitol to induce diarrhea; isotonic saline enema; Fleet's Phospho-Soda enema; and bisacodyl (Dulcolax), 10 mg, by enema or suppository. The rectal mucosa after mannitol-induced diarrhea, or after saline enema could not be distinguished from untreated rectum by proctoscopy, light microscopy, or scanning electron microscopy. Fleet's enema, and bisacodyl invariably changed proctoscopic appearances, and frequently altered light and scanning microscopic aspects. Both Fleet's enema and bisacodyl caused sloughing of surface epithelium. In addition, bisacodyl decreased the uptake of hematoxylin and eosin by crypt epithelial cells so that the affected cells had a partially erased appearance (16 of 25 biopsies examined by light microscopy). The lamina propria of 3 of these 25 biopsies contained polymorphonuclear cells. Transmission electron microscopy revealed that the abnormal crypt epithelial cells contained fewer cytoplasmic organelles and less nuclear chromatin. All lesions resolved within 7 days. Fleet's enema and bisacodyl by rectum may mislead the proctologist and the pathologist by altering normal rectal mucosa.

Bisacodyl↗

PubMed1976

Lecithin inhibits fatty acid and bile salt absorption from rat small intestine in vivo.

During digestion of a fatty meal, long chain free fatty acids (FFA) and lecithin are among the lipids solubilized in intestinal contents as mixed micelles with bile salts. We hypothesized that if lecithin were not hydrolyzed, the mixed micelles would be abnormal, and absorption of FFA and bile salts would be depressed. To test this hypothesis, isolated segments of rat small intestine were infused in vivo with micellar solutions of 2 mMolar linoleic acid and 10 mMolar taurocholate to which was added 3 mMolar 1-palmitoyl, 2-oleoyl lecithin (a common lecithin in bile and food), or 1-palmitoyl lysolecithin (the hydrolytic product of lecithin). Absorption of FFA and bile salt was measured under steady state conditions using a single-pass technique. Lecithin depressed the rate of FFA absorption by 40% (p less than 0.025) in jejunal and ileal segments whereas lysolecithin was associated with normal rates of FFA absorption. Lecithin also reduced taurocholate absorption from the ileum by 30% (p less than 0.05). These data support the idea that lecithin may depress FFA and bile salt absorption from the small intestine in pancreatic insufficiency.

Animals↗

PubMed1976

Apoprotein B in fasting and postprandial human jejunal mucosa.

We tested whether apoprotein B is present in fasting and postprandial human duodenojejunal mucosa because lipoprotein-like particles are visualized by electron microscopy within the smooth endoplasmic reticulum and the Golgi cisternae of these absorptive cells. Duodenojejunal biopsies from normal volunteers were incubated in citrate buffer and were shaken in 1% EDTA so that absorptive cells could be freed from underlying tissue. Apoprotein B was determined by double-antibody radioimmunoassay in homogenates of absorptive cells. The preparations of absorptive cells were shown to be uncontaminated by plasma lipoproteins; they did not contain any albumin by immunodiffusion able to detect 2 mug/ml. They adsorbed less than 0.1% of 125I-low density lipoprotein which was added to the citrate buffer. Cell preparations from suction biopsies of human rectum contained no detectable apoprotein B. Duodenojejunal absorptive cells from 22 fasting subjects contained 3.2 +/- 0.5 mug of apoprotein B per 100 mg (wet wt) of biopsies or 1.3 mug of apoprotein B per mg of total cell protein. The amount of apoprotein B per milligram of cell protein fell to 0.3 mug in 14 of these individuals whose mucosa was also sampled 45 min after instilling fat intraduodenally. These experiments provide immunochemical evidence that human duodenojejunal absorptive cells contain apoprotein B. This technique should be valuable for studying the physiology of intestinal lipoproteins in absorption and in patients with hyperlipidemia.

Adolescent↗

PubMed1976

Metabolism of chenodeoxycholate by intestinal mucosa.

The metabolism of 14C-labeled bile salts was studied in vitro during their absorption from infused segments of rat intestine. The transported bile salts were recovered in transudates which were collected from the serosal surface of infused segments. In the jejunum, 36% of transported [14C]deoxycholate and 48% of transported [14C]chenodeoxycholate were recovered as metabolites which migrated as a seemingly single polar compound on thin layer chromatography; 52 to 72% of these metabolites could be deconjugated by cholylglycine hydrolase to yield original [14C]deoxycholate or [14C]chenodeoxycholate, respectively. The jejunum metabolized 9 times more [14C]chenodeoxycholate than the ileum (38.1 nmoles per hr per g compared with 4.2 nmoles per hr per g), despite the fact that both segments transferred the same amount of radioactivity. In contrast, [14C]cholate, [14C]glycocholate, and [14C]glycodeoxycholate were transferred intact by the jejunum, ileum, and colon. Human jejunal and rectal mucosa were able to metabolize [14C]chenodeoxycholate to polar metabolites in vitro. Polar metabolites were also found in the portal plasma and jejunal wall 20 min after the feeding of [14C]chenodeoxycholate to bile fistula rats. It is suggested that these results complicate the interpretation of in vitro experiments on absorption of dihydroxy bile salts, and that they indicate that the human small intestine may be able to metabolize chenodeoxycholate.

Animals↗

PubMed1975

Regional differences in the effect of bile salts on absorption by rat small intestine in vivo.

1. The hypothesis that endogenous bile salts influence water absorption in rat small intestine was tested in vivo. 2. Net water transport was measured under steady-state conditions during single-pass infusion of segments from three regions of the small intestine. Each segment served as its own control. 3. Delipidated rat bile, and solutions of the principal bile salts of the rat, taurocholate and glycocholate, reduced absorption in the proximal jejunum but not in the distal ileum. 4. 1-Palmitoyl,2-oleoyl lecithin, an important biliary lecithin, counteracted the inhibitory effect of taurocholate and of glycocholate on absorption. The presence of biliary lecithins probably explains why whole rat bile did not depress water absorption in the proximal jejunum. 5. Net water transport in the distal jejunum was inversely related to log10 (taurocholate concentration). 6. Endogenous bile salts may help to maintain the fluidity of the contents of the mid-small intestine in the rat after biliary and dietary lecithins have been absorbed.

Animals↗

PubMed1975

Regional differences in oxalate absorption by rat intestine: evidence for excessive absorption by the colon in steatorrhoea.

Clinical studies suggest that steatorrhoea can be associated with excessive absorption of dietary oxalate. We examined the influence of bile salts, Ca++, and long-chain fatty acid on the absorption of oxalate and water by rat intestine in vivo. Absorption was measured under steady-state conditions during single-pass infusions. Each intestinal segment served as its own control. In jejunum, 10 mM taurocholate, the principal salt in rat bile, depressed absorption of oxalate and water. Absorption was not depressed further by Ca++ or linoleic acid. In ileum, 10 mM taurocholate did not inhibit absorption. Linoleic acid, 2 mM, depressed absorption of both oxalate and water. In colon 10 mM taurocholate decreased absorption. Net water transport was depressed further when linoleic acid was added to the infusion, but oxalate absorption was enhanced. Ca++ negated these effects of linoleic acid. It is concluded that long-chain fatty acids may enhance the absorption of oxalate from the rat colon. This observation may be relevant to understanding hyperoxaluria in patients with steatorrhoea.

Animals↗

PubMed1975

Morphological and functional effects of bile salts on rat colon.

By correlating morphological observations with quantitative measurements of net water transport, we determined whether bile salts altered colonic absorptive cells. Epithelial alteration was equivocal and water absorption was uninhibited during infusions of 1 mM deoxycholate or of concentrations of taurocholate less than 10 mM. In contrast, 3 mM deoxycholate and greater than 10 mM taurocholate caused severe altertion of colonic epithelium and inhibited water absorption. These studies suggest that bile salts in the low concentrations normally found within the colon have little effect on colonic structure or water absorption. On the other hand, abnormally high concentrations of bile salts do alter colonic mucosal structure and function.

Animals↗

PubMed1975

Effect of dioctyl sodium sulfosuccinate on structure and function of rodent and human intestine.

We tested the hypothesis that dioctyl sodium sulfosuccinate (DSS), an anionic detergent often described as a stool softener, blocks water absorption in the small and large intestines. Net water transport was measured under steady state conditions in vivo during single pass infusions of intestinal segments; each segment served as its own control. DSS, in concentrations which may obtain when it is fed in segments of rat jejunum, ileum, or colon. In man, 0.5 mM DSS inhibited water absorption by 80%. In rats, the degree of inhibition was linearly related to log10 of the concentration of DSS (0.1 to 2.0 mM). Furthermore, DSS altered the histological appearance of the surface absorptive cells of the rat colon. Because of these properties, DSS could be regarded as a stimulant laxative.

Animals↗

PubMed1975