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The model proposed by Diamond and Bossert [1] for isotonic water transport has received wide acceptance in recent years. It assumes that the local driving force for water transport is a standing osmotic gradient produced in the lateral intercellular spaces of the epithelial cell layer by active solute transport. While this model is based on work done in absorptive epithelia where the closed to open direction of the lateral space and the direction of net transport are the same, it has been proposed that the lateral spaces could also serve as the site of the local osmotic gradients for water transport in secretory epithelia, where the closed to open direction of the lateral space and net transport are opposed, by actively transporting solute out of the space rather than into it. Operation in the backward direction, however, requires a lower than ambient hydrostatic pressure within the lateral space which would seem more likely to cause the space to collapse with loss of function. On the other hand, most secretory epithelia are characterized by transport into a restricted ductal system which is similar to the lateral intercellular space in the absorptive epithelia in that its closed to open direction is the same as that of net transport. In vitro micropuncture studies on the exocrine pancreas of the rabbit indicate the presence of a small but statistically significant increase in juice osmolality, 6 mOsm/kg H(2)O, at the site of electrolyte and water secretion in the smallest extralobular ducts with secretin stimulation which suggests that the ductal system in the secretory epithelia rather than the lateral intercellular space is the site of the local osmotic gradients responsible for isotonic water transport.
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PMID:Isotonic water transport in secretory epithelia. 33 93

The effects of secretin, the physiological secretagogue for pancreatic ducts, were studied in CAPAN-1 pancreatic duct carcinoma cells. When grown to confluence on plastic dishes, CAPAN-1 cells form domes and exhibit marked increases in culture content of Na+ and urea distribution space (UDS). This parameter is measured as an index of both intracellular and dome compartments under the conditions adopted. Both Na increase and dome formation are inhibited by long term incubation with phorbols, DIDS, DPC, EIPA, H2DIDS, and brefeldin. Short term treatment with secretin or 8-Br-cAMP/teophylline causes dome collapse and a marked decrease in UDS and culture content of Na. Secretin-induced sodium decrease is not abolished by ion channel inhibitors, suggesting that diffusion routes other than ion channels are involved in hormone effects. This hypothesis is also in agreement with data obtained on CAPAN-1 cells cultured on permeable inserts, where no change in Na content or UDS is detected upon secretin treatment. Confluent monolayers exhibit a high transepithelial resistance (Rms) which is markedly and reversibly decreased by secretin. The hormone also decreases the transepithelial voltage (Vms) and raises the monolayer permeability to mannitol. It is concluded that secretin enhances the paracellular permeability of pancreatic duct cells. This effect of secretin, unknown thus far, may be involved in the mechanism of pancreatic secretion in vivo.
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PMID:Secretin increases the paracellular permeability of CAPAN-1 pancreatic duct cells. 1084 94

Magnetic resonance (MR) cholangiopancreatography (MRCP) is widely used in the evaluation of pancreatobiliary disorders. However, numerous related pitfalls may simulate or mask pancreatobiliary disease. Maximum-intensity-projection (MIP) reconstructed images completely obscure small filling defects and may demonstrate respiratory motion artifacts. T2 weighting may vary with different MR imaging sequences and influence MRCP findings. Incomplete imaging may create confusion regarding ductal anatomy or disease. Furthermore, MRCP yields only static images and thus may fail to depict various anomalies. Limited spatial resolution makes differentiation between benign and malignant strictures with MRCP alone extremely difficult. Susceptibility artifacts may be caused by metallic foreign bodies or gastric-duodenal gas. Fluid accumulation may produce a pseudolesion or pseudostricture, although changing the imaging angle or section thickness may be helpful. Pneumobilia may be misinterpreted as bile duct stones, and true stones may be overlooked. Pulsatile vascular compression can cause pseudo-obstruction of the bile duct. Use of both source and MIP reconstructed images obtained from different angles can help avoid cystic duct-related pitfalls. Repeat MRCP or conventional MR imaging can help avoid pitfalls related to the periampullary region. Segmental collapse of the normal main pancreatic duct may be misinterpreted as stenosis, but administration of secretin is helpful. An awareness of these pitfalls and possible solutions is crucial for avoiding misinterpretation of MRCP images.
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PMID:Pitfalls in MR cholangiopancreatographic interpretation. 1115 41

Closed duodenal loops may be made in dogs by ligatures placed just below the pancreatic duct and just beyond the duodenojejunal junction, together with a posterior gastro-enterostomy. These closed duodenal loop dogs die with symptoms like those of patients suffering from volvulus or high intestinal obstruction. This duodenal loop may simulate closely a volvulus in which there has been no vascular disturbance. Dogs with closed duodenal loops which have been washed out carefully survive a little longer on the average than animals with unwashed loops. The duration of life in the first instance is one to three days, with an average of about forty-eight hours. The dogs usually lose considerable fluid by vomiting and diarrhea. A weak pulse, low blood pressure and temperature are usually conspicuous in the last stages. Autopsy shows more or less splanchnic congestion which may be most marked in the mucosa of the upper small intestine. The peritoneum is usually clear and the closed loop may be distended with thin fluid, or collapsed, and contain only a small amount of pasty brown material. The mucosa of the loop may show ulceration and even perforation, but in the majority of cases it is intact and exhibits only a moderate congestion. Simple intestinal obstruction added to a closed duodenal loop does not modify the result in any manner, but it may hasten the fatal outcome. The liver plays no essential role as a protective agent against this poison, for a dog with an Eck fistula may live three days with a closed loop. A normal dog reacts to intraportal injection and to intravenous injection of the toxic substance in an identical manner. Drainage of this loop under certain conditions may not interfere with the general health over a period of weeks or months. Excision of the part of the duodenum included in this loop causes no disturbance. The material from the closed duodenal loops contains no bile, pancreatic juice, gastric juice, or split products from the food. It can be formed in no other way than by the activity of the intestinal mucosa and the growth of the intestinal bacteria. This material after dilution, autolysis, sterilization, and filtration produces a characteristic effect when introduced intravenously. When in toxic doses it causes a profound drop in blood pressure, general collapse, drop in temperature, salivation, vomiting, and profuse diarrhea, which is often blood-stained. Splanchnic congestion is the conspicuous feature at autopsy and shows especially in the villi of the duodenal and jejunal mucosae. Adrenalin, during this period of low blood pressure and splanchnic congestion, will cause the usual reaction when given intravenously, but applied locally or given intravenously it causes no bleaching of the engorged intestinal mucosa. Secretin is not found in the duodenal loop fluid, and the loop material does not influence the pancreatic secretion. Intraportal injection of the toxic material gives a reaction similar to intravenous injection. Intraperitoneal and subcutaneous injections produce a relatively slow reaction which closely resembles the picture seen in the closed duodenal loop dog. In both cases there is a relatively slow absorption, but the splanchnic congestion and other findings, though less intense, are present in both groups. There seems, therefore, to be no escape from the conclusion that a poisonous substance is formed in this closed duodenal loop which is absorbed from it and causes intoxication and death. Injection of this toxic substance into a normal dog gives intoxication and a reaction more intense but similar to that developing in a closed-loop dog.
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PMID:INTESTINAL OBSTRUCTION : I. A STUDY OF A TOXIC SUBSTANCE PRODUCED IN CLOSED DUODENAL LOOPS. 1986 44