An additional protein in rat pancreatic juice has been observed, which is present in healthy rats after pancreatic duct cannulation or in rats in which experimental pancreatitis has been induced by either cerulein or taurocholate. The protein appears ½-1 day after surgery or onset of pancreatitis, is present for the following 3–4 days and disappears afterwards. It is found in pancreatic homogenate or in zymogen granules from rats with pancreatitis, but not in normal rats. It does not seem to be related to the recently described ‘pancreatic stone protein’. We would like to refer to this protein as ‘pancreatitis-associated protein’.

The influence of feeding isocaloric diets containing either 65% of fructose (F 65) on 65% of glucose (G 65) were studied on the uptake of both sugars in segments of rat proximal jejunum and distal ileum. The hexose absorption was compared to that obtained in animals receiving isocaloric amounts of a diet containing 30% of glucose (G 30). Feeding fructose (F 65) for 3 days resulted in a 2.5-fold increase of fructose uptake in the jejunum and a 40% increase in the ileum as compared to group G 30. When fructose (F 65) was administered instead of G 65 the uptake of fructose was enhanced by 75% in the jejunum and 35% in the ileum. Stimulation of glucose absorption in segments of the proximal and distal small intestine by diets F 65 and G 65 was nearly identical as compared to the values of group G 30. The stimulation of the uptake of fructose induced by fructose feeding parallels an adaptive increase in the activity of enzymes involved in fructose metabolism in the mucosa of the small intestine.

The existence of a region of low pH juxtaposed to the proximal jejunum has been proposed to explain anomalies in the transfer of weakly-ionizing substances: yet no direct evidence for this layer exists. Surface electrode studies on everted sacs revealed the existence of the layer and estimated the pH to be at least 5.5 when the buffer pH is 7.2. With 60 μ m long tip microelectrodes, a value of 6.0 was obtained, however, the dimensions of this microclimate are uncertain. Optical experiments with pH-indicators using a microscope of 20 μ m resolving power and flat strips in vitro , failed to detect this layer. With the dimensions of the tip microelectrode known, values are given for the maximum possible microclimate pH for a corresponding microclimate depth. The significance of the pH microclimate to malabsorption is briefly discussed.

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SUMMARY Experiments were carried out in different segments of the intestine of unanaesthetised rats to assess the effect of vasopressin on intestinal absorptive processes. The following data were observed.(1) Within a physiological range of doses (Aziz, 1969), ADH diminished the net sodium absorption mainly by reducing the unidirectional sodium influx, whereas the behaviour of the efflux was not uniform. (2) The unidirectional volume fluxes showed the same behaviour as did the sodium fluxes. (3) ADH produced an oral-aboral gradient (jejunum > ileum > colon). (4) ADH did not significantly change the transfer of actively transported sugars; it did influence, however, passively transported substances. (5) During the intravenous application of ADH, a substance was secreted into the perfusion solution which diminished the absorption of volume and electrolytes. (6) Cyclic AMP acted on intestinal absorption in the same way as did ADH. In view of these results two mutually independent transport pathways for sodium and water are supposed, one of which is influenced by ADH or cAMP. Based on a two membrane model, an ADH mechanism is discussed: the permeability of the luminal membrane system is enhanced in the presence of vasopressin.Vasopressin, the antidiuretic agent of the neurohypophysis, changes the permeability of several epithelial structures, including the intestinal mucosa, and possibly controls the transport mechanism and permeability of such boundaries. This was shown by physiological doses applied to the small intestine of man (Soergel et al., 1968) and rats (Dennhardt and Haberich, 1972). These doses produced a decrease of both the net sodium and the net water transport. The kind of effect that was produced by ADH on the intestinal membrane structures, however, remained unclear.In the present series of experiments on intestinal segments we examined the influence of ADH upon the unidirectional fluxes of sodium and water, as well as the transport rates of glucose, fructose, 3-0-methyl-glucose, and urea. For this purpose, we had to work out an experimental procedure which allowed experiments on unanaesthetised rats because it is well known that anaesthetics enhance endogenous vasopressin levels (Bonjour and Malvin, 1970 MethodsThe experiments were carried out on intestinal segments of the jejunum and the colon of Wistar II rats weighing between 200 and 250 g. The animals were operated on at least three days before the beginning of the experiments. An inflatable cuff was placed at each end of a chosen intestinal segment, so that a particular intestinal segment of about 10 cm in length could be temporarily isolated and subsequently perfused by means of a tube placed at the proximal end and an outlet tube anastomosed to the distal end of the gut segment. All tubes came out on the animal's back and were protected by a semicircular piece of metal. The chosen intestinal segment was perfused by means of a peristaltic pump (Harvard Corp.) under recirculation conditions ('closed system'). Figure 1 illustrates the experime...

1. Indwelling non-occlusive catheters were placed in the vena porta and inferior vena cava of female rats several days before experimentation. Isotonic saline or isosmotic glucose (2% of body wt.) was infused into one vein followed one to several days later with an identical infusion into the other vein of each conscious animal. 2. Significantly higher urine flow and sodium excretion resulted from infusion of isotonic saline (0.5 ml/min) into the vena porta than into the vena cava. Modest prehydration or section of the hepatic branch of the right vagus did not affect the differential sodium response. Changes in endogenous creatinine clearance and potassium excretion were not significantly different for the two routes. Mean values for net peak sodium excretion and contemporaneous urine flow, urinary sodium concentration, and fractional sodium excretion were significantly higher for the portal than for the caval infusion while differences in glomerular filtration rate and filtered sodium load were insignificant. No significant difference in sodium excretion resulted from infusion of isosmotic glucose by the two routes. 3. Compared to the response promoted by the isotonic saline load infused at 0.5 ml/min, the differential response in sodium excretion was prolonged when the same load was infused at 0.375 ml/min. Sodium excretion was not significantly different for the two routes when the same isotonic saline load was infused at 0.75 ml/min. 4. These experiments provide evidence for participation of the liver in the control of sodium excretion and suggest release of a hepatic humoral factor which may be controlled by the duration of exposure of the hepatic circulation to an adequate load of isotonic saline.