The effect of a high osmotic solution on active and passive sugar permeation was investigated in 19 healthy volunteers. The reduced rate of active sugar absorption (3-O-MG and xylose) out of a high osmotic solution was interpreted as a consequence of an impaired emptying of the stomach. The increased passive permeation of intact disaccharides applied in hyperosmolar solution demonstrates an increased gastrointestinal permeability. Intubation studies suppose increased disaccharide absorption out of hyperosmolar solution in the stomach, i.e. high osmolar solutions increase gastric mucosal permeability.

Antrectomy reduced the levels of circulating gastrin but did not change jejunal morphology. In vitro and in vivo absorption as well as the activity of some brush border enzymes were increased. The observed alterations are discussed on the basis of antrectomy-induced alterations in the release of gastrointestinal hormones, gastric and pancreatic secretion and gastric emptying.

The present review tries to coordinate anatomical barriers and the biochemical and immunological events controlling and even preventing the entry of substances from the external environment into the extra- and intra-cellular space of the body. A selection of diseases with disturbance of the "barrier function" is included.

Age-related changes in the gut were investigated in male gnotobiotic rats, living in a controlled and constant environment until death. Parameters of the regenerative compartment of the jejunum and ileum were the cell production rate (measured by a stathmokinetic technique), the number of crypts, and the crypt:villus ratio. Parameters of the functional compartment were the average surface area of the villi, height and broadness of villi, etc. Age did not change the size of individual villi or crypts or the cell production rate. The number of crypts and, to the same extent, the number of villi increased with age, indicating a continuation of mucosal growth up to an age of 2 yr.

Feeding an elemental diet (Vivonex) to rats over 9 days causes a decrease in the rate of cell renewal and a reduction in villus size in both the jejunum and ileum, as compared with rats fed regular chow. The addition of bulk to elemental diet cannot prevent the reduction in villous size, but it can cause a small increase in the rate of cell renewal, which is still much lower than that in chow-fed rats. The serum gastrin level of rats fed the elemental diet is about one-third of the level found in chow-fed rats, and it is not changed by the addition of bulk.

After an oral load of 10 g polyethylene glycol, its concentration in the urine was measured by gas chromatography. The coefficient of variation of the imprecision between run was about 11%. The urinary excretion was 25% of the administered dose with a coefficient of variation of the interindividual variation 26% and the intraindividual variation between 13% and 29%.

Isolated, partially purified or enriched rat gastric muscosal parietal cells were shown to respond to carbamycholine (EC50 = 2 μM) and other muscarinic cholinergic agonists as measured by an increased accumulation of 14C-aminopyrine, an indirect measure of acid secretion. The secretory response to carbamylcholine was shown to be inhibited stereoselectively and reversibly by nanomolar concentrations of muscarinic cholinergic antagonists. Non-muscarinic antagonists, including cimetidine, were either ineffective or very weak inhibitors. The affinity constants calculated for cholinergic antagonist inhibition of 14C-aminopyrine accumulation induced by carbamylcholine were similar to those previously calculated from direct binding studies on purified parietal cell particulate fractions using 3H-QNB (1). These studies support the existence of specific parietal cell muscarinic cholinergic receptors with which the natural secretagogue acetylcholine interacts to regulate gastric acid secretion.

The tritiated muscarinic cholinergic antagonist quinuclidinyl benzilate, [3H]QNB, was used as a direct probe for the detection and characterization of muscarinic cholinergic receptors associated with the particulate fraction of isolated and purified rat gastric muscosal parietal cells. Specific binding is saturable (Bmax = 55 fmol/mg protein, KD = 0.78 nM), shows a single population of binding sites, and has appropriate pharmacological specificity. Nanomolar concentrations of muscarinic cholinergic antagonists, such as atropine and scopolamine, inhibit [3H]QNB binding by 50%, whereas micromolar concentrations are needed for agonists, such as acetylcholine, oxotremorine, and carbamylcholine. Binding is also stereoselective as shown by the more than 1,000-fold difference in inhibitory potencies of the stereoisomers of benzetimide. Noncholinergic agents, including pentagastrin, histamine, and the H2-receptor antagonists cimetidine and metiamide, have little or no effect on [3H]QNB binding at concentrations of 100 microM. These data support the existence of specific parietal cell muscarinic cholinergic receptors with which the secretagogue acetylcholine may directly interact to initiate gastric acid secretion.

Starvation for 48 hrs reduced the activity of sucrase referred to unit length in rat proximal small intestine by approximately 30%, irrespective of whe her mucosal scrapings, isolated villus epithelial cells or brush border membranes were investigated. Sucrase activity referred to unit weight, unit protein or to unit DNA of intestinal epithelium did not change.

A modified Roux-en-y repositioning of rat proximal small intestine resulted in a gut segment (A) exposed only to digestive secretions, but not to food and a gut segment (B) exposed to food, stomach juice and by reflux only to digestive secretions, and a third segment (C) exposed to both, food and digestive secretions. The changes in segment A were qualitatively very similar to those occurring after removal of luminal nutrition (intravenous feeding, self-emptying blind loop, and Thiry Vella loop). These findings support the hypothesis that the presence of luminal nutrition is a major factor regulating mucosal mass and enzyme activity in rat proximal small intestine. The changes in the luminal environment in segment B caused an increase in mucosal mass (in the proximal half only), an increase in sucrase activity which paralleled the increase in mucosal mass, and no change in activity of alkaline phosphatase which in fact was a decrease in activity `at the cellular level'. Later on the net absorption of sodium and potassium was improved and the disappearance of galactose was unchanged when referred to unit length of small intestine. In segment C there was a small increase in mucosal mass, an increase in activity only for alkaline phosphatase, and an improvement of the net absorption of sodium without changes in the disappearance of galactose. These changes were compatible with a more proximal promotion of a distal gut segment.

Starvation overnight and starvation for 48 h reduced the weight and the protein content of mucosal scrapings, but only minimally reduced the DNA content of the mucosal scrapings. The activity of sucrase and maltase was reduced by both periods of starvation. The activity of lactase and of acid and alkaline phosphatase, however, was less subject to starvation. There were striking differences in the response to starvation between the proximal, mid and distal third of the small intestine. The importance of the proper reference system was discussed.

Zytostatika hemmen nicht nur die Proliferation von Tumorzellen sondern auch die Proliferation im Dünndarmepithel. Die Folge davon ist eine Zellverarmung und Zellschädigung die zu einer Funktionsminderung führen. Bedingt durch die enorme Reservekapazität des Dünndarmepithels tritt diese Funktionsminderung meist erst nach extrem hohen Einzeldosen oder nach hochdosierter Mehrfachgabe von Zytostatika klinisch in Erscheinung.