Immunofluorescent localization of cyclic AMP in human jejunum and rat liver and jejunum.
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1. The utilization of some metabolic fuels has been measured in vitro in a preparation of rat jejunum to which the substrates were supplied via the perfusate flowing through the vascular bed. 2. In jejunum from 48 hr-fasted rats, the combined rates of utilization of 1 mM-acetoacetate and 2mM-D-3-hydroxybutyrate are similar to that of 7.5 mM-glucose. 3. The utilization of glucose is reduced in jejunum from animals fasted for 48 hr (45--63% reduction) and also from animals after 3--6 days of diabetes induced by streptozotocin (29% reduction). The addition of ketone bodies or of Na-oleate to the vascular perfusate does not reduce the utilization of glucose by the jejunum of either fed or 48 hr fasted rats. 4. Ketone bodies in the vascular perfusate reduce the oxidation of glucose by the jejunum of fed rats. In the jejunum of 48 hr-fasted rats, ketone bodies completely inhibit the oxidation of glucose so that all the glucose utilized by the tissue is converted to lactate. 5. The findings are discussed in relation to other work and it is concluded that substrates for the oxidative metabolism of the jejunum of fasted rats are likely to be ketone bodies, glutamine and fatty acids; at the same time the utilization of glucose is reduced and its oxidation completely abolished.
Acute, isolated loops of proximal and distal jejunum of weanling swine were exposed to either heat stable porcine Escherichia coli enterotoxin, heat labile porcine Escherichia coli enterotoxin, cholera toxin or theophylline. Unidirectional sodium fluxes in response to heat stable in the proximal jejunum were dependent on the length of time that the intestinal mucosae was exposed to the enterotoxin. Net water, sodium and chloride and unidirectional sodium and chloride flux measurements in the proximal jejunum in response to each agent uniformly indicated that net secretion of fluid and electrolytes was the result of increased unidirectional sodium secretion or blood-to-lumen flux and decreased unidirectional chloride absorption or lumen-to-blood flux. In addition heat stable cholera toxin and theophylline but not heat labile decreased unidirectional chloride secretion a small but significant amount in the proximal jejunum. Sodium and chloride flux measurements in the distal jejunum demonstrated that all four secretory agents could stimulate net secretion of water, sodium and chloride in that region. The response to these secretory agents as measured by sodium and chloride unidirectional flux rates was not similar to changes observed in the proximal jejunum. In the distal small intestine, whereas heat labile cholera toxin and theophylline induced similar qualitative changes in unidirectional sodium and chloride fluxes, that induced by heat stable differed.
1 Anesthetized rats (225 to 300 g) were used to study the inhibitory effect of morphine on fluid secreted by the small intestine. 2 Small intestinal fluid secretion was stimulated by infusion of prostaglandin E1 (PGE1) into the aortic arch, the jejunum being more sensitive than the ileum. Infusion of PGE1 2 microgram/min caused maximal net fluid secretion in the jejunum but inhibited net fluid absorption in the ileum. 3 Morphine caused a dose-related inhibition of maximal PGE1-stimulated fluid secretion in the jejunum. At the higher doses of morphine used (5 to 20 mg/kg) the fluid transporting function of the jejunum was restored almost to normal net absorption. 4 The inhibitory effect of morphine on PGE1-stimulated fluid secretion was antagonized by naloxone. Naloxone caused a parallel shift to the right of the dose-response curve for morphine. 5 Two other narcotic analgesics were assayed relative to morphine and their descending order of potency was oxymorphone greater than morphine greater than pethidine. 6 It is suggested that the antisecretory effect of morphine in the small intestine may contribute to its efficacy as an anti-diarrhoeal drug. Further studies on the rat jejunum may show it to be a useful model for predicting narcotic drug activity and as such, may give some insight into the mechanisms of action of these drugs.
The quantitative passage of urea-N and ammonia N into an isolated jejunum of the merino sheep was studied within one hour before, and 1, 2, 3, 4 and 5 hours after feeding. The total amount of ammonia-N that passes to the isolated jejunum [to both proximal and distal part] within an hour is small [0.28-0.35 mg h-1], without any significant differences in passage prior to and after feeding. However, urea-N secretion is high, especially secretion to the fore part of the jejunum [ 3.35-3.62 mg h-1]. The passage of urea-N to the rear part of the jejunum is about 1/3 lower than passage to the fore part. Urea solution of higher concentration than in peripheral blood was incubated in the isolated jejunum to study an adverse phenomenon: absorption of urea from intestinal lumen to the blood. The levels of urea in peripheralblood and in incubate reached a balance state within one hour after administration. The data obtained testify to the permeability of the wall of the gut for urea in both directions.
1. This paper describes an investigation of the kinetics of influx of the dipeptide glycylsarcosine and the amino acids glycine and L-leucine into rings of everted hamster small intestine in vitro, in proximal and distal small intestine (jejunum and ileum). Results were expressed per unit wet weight of intestine. 2. At all concentrations studied (0.1--100 mmol/l), influx of glycylsarcosine was more rapid in the jejunum than in the ileum. In contrast, at all concentrations studied, influx of glycine and leucine was more rapid in the ileum than the jejunum. 3. Estimates of the simple diffusion component in total influx were made. This component became increasingly large as the substrate concentration was raised. After correction for simple diffusion, transport of all three substrates conformed to Michaelis-Menten kinetics in both jejunum and ileum. Values for simple diffusion, apparent Kt and Vmax, are reported. 4. Possibly physiological implications of the results are discussed, and it is pointed out that under experimental conditions similar to our own, simple diffusion is too large a component in total influx to be ignored.
An experimental study was conducted on the effect of resection of the jejunum and ileum on gastrin release. The intravenous infusion of L. arginine in a dose of 0.5 g per kg body weight for 30 minutes proved to be most practical in evaluating gastrin release in addition to insulin and glucagon release. Serum gastrin levels in response to this dose of arginine were determined before and three weeks, three months and one year after resection of the jejunum and of the ileum. At three weeks, a significant increase in gastrin levels occurred in bothe the fasting state and after stimulation in dogs with either jejunum or ileum resection. At three months, the elevated gastrin response persisted only in those with jejunum resection. By one year, the gastrin levels had fallen in almost all dogs to approximately the preoperative levels.
The influence of intravenously administered synthetic salmon calcitonin on water, electrolyte and calcium fluxes in in vivo rabbit jejunum and ileum was examined. Rabbits were divided into four groups: those receiving (1) saline intravenously while a glucose-free isotonic saline solution perfused the jejunum and ileum; (2) calcitonin intravenously while the same intestinal perfusate was used as in group 1; (3) intravenous saline while 10 mM glucose-isotonic saline solution perfused jejunum and ileum; and (4) intravenous calcitonin while the intestinal perfusate was of the same composition as in group 3. Calcitonin provoked a significant increase in jejunal and ileal water, sodium, and bicarbonate secretion in both the glucose-free and glucose-containing perfusate groups. No influence on calcium movement was noted. These results, similar to findings of Gray et al. (J Clin Invest 52:3084-3088, 1975) in human jejunum, suggest that calcitonin may play a role in the pathogenesis of the watery diarrhea noted in about one-third of patients with medullary carcinoma of the thyroid. In addition, these studies demonstrate the usefulness of the rabbit as an animal model with which to investigate further the effects of calcitonin upon intestinal fluid and electrolyte transport.
We studied the effect of ethanol on glucose and water absorption in vivo. In preliminary experiments, using sodium amytal anesthesia, we found that control animals, whose jejunal segment was perfused without ethanol, required more anesthetic agent than those perfused with ethanol. Thus, to allow for unbiased comparison of the absorption data between the two groups of animals, all absorption studies were carried out on conscious restrained hamsters. We found that ethanol did not influence the permeability of the jejunum to polyethylene glycol (PEG) and meglumine diatrizoate. In addition, ethanol did not influence the time required for the onset of steady-state absorption. Using both the gravimetric and the electrical methods, we were unable to show any measurable osmotic pressure exerted by ethanol (150-1050 mM) on the hamster jejunum. In the absorption studies we found that perfusion of the hamster jejunum with five increasing concentration of ethanol (450-1050 mM) appeared to cause a concentration-dependent depression in steady-state glucose transport. Water transport was depressed only when 4.8% (1050 mM) ethanol was perfused.
In order to study the morphological effects of exposure of the jejunum to low ethanol concentrations, we perfused hamster jejunum with 2.1-4.8% ethanol. Following 45 min exposure, many of the villi developed fluid-filled blisters. To compare these findings to the effect of an inert solute at similar concentrations, we perfused hamster jejuna with mannitol. This caused necrosis of the villus tips but no blister formation. Therefore the blisters were the result of the action of ethanol. The rat jejunum was less resistant to ethanol than that of the hamster. We suggest that the initial insult of the freely permeant ethanol is deep to the epithelium, resulting in accumulation of edema under the epithelium.
Total gastrectomy was performed on purebred beagle dogs and a 30--40 cm jejunal segment was grafted isoperistaltically between oesophagus and duodenum. Histological and histoautoradiographical examinations were carried out and the wall-thickness and the cell-transformation rate in the interponate determined. Despite the isoperistaltic substitute-stomach a muscular wall-hypertrophy of 140% of the interponated jejunum was found. The reason for this hypertrophy is thought to be the result of adhesions and the functional mechanical demands. Histoautoradiographical examinations confirmed that the regeneration time in the substitute-stomach decreased by 70% compared with the normal jejunum. The distinct reduction of cell regeneration in the regeneration in the interponated jejunum could be attributed to the considerable regression of the absorbent performance and to the increase in its mechanical exercises.
The effect of Ca++ on jejunal osmiophilic particles was studied in a recirculating system which was not contaminated with plasma lipoproteins. An isolated, infused segment of rat jejunum was suspended in a bath of liquid paraffin. Transudate, containing osmiophilic particles, appeared like beads of sweat on the serosal surface, and fell to the bottom of the bath. In the range of 25-38 C, 30 C proved to be optimal for histological preservation of villous architecture. Production of transudate, 20 mg/min/g of jejunum, and transport of [14C] oleate proceeded nearly linearly after the first 30 min. Necrosis of mid-villus and crypt cells became obvious by light microscopy after one hour. Therefore, transudate was collected between the period of 30-60 min. Shadow casting of transudates, produced when saline was infused, revealed that 86 +/- 9 (SD) % of osmiophilic particles was less than 800 A in diameter; 13 +/- 8% was 800-1000 A; 0.4 +1- 0.5% was 1000 - 2000 A. Corresponding values were 58 +/- 10, 25 +/- 5, and 16 +/- 5% when 5 mM [14C] oleate + 2.5 mM monoolein was infused; 75% of the transported [14C] appeared in triglyceride. Adding 2 mM Ca++ to the infusion doubled the transport of [14C] triglyceride without increasing particle size further. We conclude that luminal Ca++ increases the absorption of luminal fatty acid by rat jejunum in vitro.
Rabbit ileal, jejunal, and duodenal loops were exposed to purified enterotoxin from Clostridium perfringens type A and then perfused for comparative analysis of effects of the enterotoxin on each region of the intestine. Ileal loops responded with enhanced net secretion of fluid and sodium, inhibition of chloride and glucose uptake, and substantial sloughing of epithelial cells. The jejunum responded with fluid secretion, enhancement of sodium secretion only during the first 20 min, inhibition of chloride and glucose uptake, and substantial sloughing of epithelial cells. In the duodenum, transport of fluid, sodium, and chloride was significantly altered only during the first 20 min of perfusion, and significant inhibition of glucose uptake varied from one period to another. Epithelial damage was much less than that seen in the jejunum or ileum. Levels of fluid protein in all three sections corresponded closely to extent of tissue damage. In general, it was found that the severity of response to fixed doses of enterotoxin varied as follows: ileum greater than jejunum greater than duodenum.
The dog jejunum is a much denser tissue than the ileum, with a greater weight per unit length and higher proportion of mucosal tissue. Morphometric analysis reveals longer and wider villi, deeper crypts and larger enterocytes in the jejunal mucosa. Uptake of phenylalanine or beta-methyl-glucoside by tissue slices in vitro is slightly greater in jejunal than in ileal tissue. The levels of acid phosphatase and alkaline phosphatase in the individual enterocytes are significantly greater in the jejunum, according to quantitative histochemical analysis. The absorption of water, sodium, potassium, chloride and glucose in vivo is significantly smaller in the jejunal than in ileal loops, particularly when expressed in terms of unit mucosal weight. Sodium and water absorptions are stimulated by glucose at both sites, but the stimulation is significantly greater in the ileum. Opposite results have been obtained in rats where the transport of phenylalannie in vitro is greater in the ileum, but water, electrolyte and glucose absorption in vivo is greater in the jejunum.
During osmotic diarrhea, loss of water and electrolytes appears to be greater in infants than in adults. In 2-, 3-, and 7-wk-old rats, we studied net transport of H(2)O, Na, and Cl, during in vivo perfusion of segments of the jejunum and ileum, from solutions with osmolalities of 300, 375, 500, or 700 mosmol/kg. In the jejunal segments, from the hypertonic solutions net transport of H(2)O, Na, and Cl was into the lumen and greater in the 2- than 7-wk-old rats. In the ileal segments, transport of water was into the lumen, transport of Na was minimal and variable, whereas transport of Cl was usually out the lumen. In 3-wk-old rats, transport rates were intermediate between those in 2- and 7-wk-old rats. The calculated filtration coefficient (microliters of H(2)O transported per hour per unit osmolality gradient-lumen-serum-per gram dry weight) of water suggested that the resistance to water flow did not increase with rise in luminal hypertonicity in the jejunum of the 2- and 3-wk-old rats, whereas in jejunum of the 7-wk-old rats and in ileum of rats in all three ages, the resistance to water flow increased with the rise in luminal osmolality. The differences in the transport rates and the resistance to water flow, between segments of the 2-, 3-, and 7-wk-old rats, suggested a maturational phenomenon that appears to continue beyond the 3rd wk of life and could have been due to differences in some physical property of the mucosal membrane.
By using the jejunal tract of rat and hamster intestine, net fluid transintestinal transport in the everted sac incubated in vitro at 28 degrees C and at 38 degrees C has been determined. In the scraped mucosa wet weight/dry weight ratio, cell water, sodium and potassium concentration have been detected in vivo and in vitro, throughout the incubation time, at the two different temperatures. Under all these conditions ATP, ADP and AMP levels have been determined in total intestine and in scraped mucosa. In rat jejunum incubated in vitro at 38 degrees C transintestinal fluid transport continuously decreases during 1-h experiment; in the same time the enterocyte gains sodium, dilutes cell potassium and swells, whereas its energy charge is dramatically reduced. All these parameters are constant in rat jejunum incubated at 28 degrees C and in the hamster incubated both at 28 degrees C and at 38 degrees C throughout the experiment. An inadequate diffusion of oxygen into the enterocyte, could tentatively explain experimental results obtained on rat jejunum at 38 degrees C. Under all tested conditions, energy charge and intracellular potassium are lower in conditions in vitro than in those in vivo; the contrary happens for cell sodium and swelling. The oxygenation of the intestine in vitro, lower than the one in vivo, could explain the different behaviour found in the two experimental conditions.
A case of histoplasmosis of the jejunum is presented. This is apparently the first reported case of African histoplasmosis primarily affecting the jejunum. Grossly, there was stricture formation together with tubercles scattered over the surface of the bowel and adjoining mesentery. Also the mesenteric lymphnodes were enlarged. It is therefore difficult to distinguish jejunal histoplasmosis from tuberculosis, carcinoma and lymphoma of the jejunum and diagnosis can only be based on the demonstration of the characteristic yeast cells from the specimen.