Duodenum In Response Research Articles

Effects of verapamil and dexamethasone on the 1,25-dihydroxyvitamin D 3-mediated calcium absorptive mechanism in the organ-cultured embryonic chick duodenum

1,25-Dihydroxyvitamin D 3 (1,25(OH) 2D 3) is known to induce the biosynthesis of a specific, calcium-bincling protein (CaBP) and to stimulate calcium transport in the organ-cultured embryonic chick duodenum. The biosynthesis of CaBP has been shown previously to exhibit an absolute dependence on the ambient calcium concentration of the culture medium. Verapamil, a calcium-channel blocker, decreased calcium influx into the organ-cultured duodenum and inhibited the induction of CaBP by 1,25(OH) 2D 3. Raising ambient calcium concentrations to as high as 10 mM did not prevent or reverse the inhibitory actions of verapamil. Dexamethasone, known to augment CaBP biosynthesis and calcium uptake in the organ-cultured duodenum in response to 1,25(OH) 2D 3, largely prevented inhibition of CaBP by verapamil. The actions of verapamil and dexamethasone were correlated with altered steady-state calcium concentrations of the organ-culture duodenum, strongly supporting a regulatory role of calcium in the 1,25(OH) 2D 3-mediated, intestinal calcium absorptive mechanism.

Opiate nerves mediate feline pyloric response to intraduodenal amino acids.

Intraluminal pressures and myoelectric activity were recorded from the feline antrum, pylorus, and duodenum in response to intraduodenal amino acid solutions. Mixed amino acids (0.02 mg/ml, 3.0 ml) increased the amplitude of pyloric contractions (59.7 +/- 7.9 mmHg) and pyloric spike activity (73.7 +/- 6.8% of slow waves with spike activity) compared with a saline control (P less than 0.001). The selectivity of these responses was determined with specific amino acids. L-Tryptophan (10 or 40 mM) produced a response similar to the mixed amino acid response, while L-phenylalanine or L-glycine (10 or 40 mM) had no effect. Intra-arterial tetrodotoxin, intraluminal ethyl aminobenzoate, or intravenous naloxone (1.0 mg/kg) abolished the pyloric responses to amino acids (P less than 0.02). Bilateral cervical vagotomy had no effect. Cholecystokinin octapeptide (CCK-OP) produced dose-dependent increases in the amplitude of pyloric contractions and in pyloric spike activity. The ED50 dose of CCK-OP (1.0 microgram/kg iv) gave an increase in pyloric pressure of 155.6 +/- 49.9 mmHg and in spike activity of 77.7 +/- 9.4%, similar to mixed amino acids or tryptophan. These effects of CCK-OP were not antagonized, however, by a dose of naloxone (1.0 mg/kg) that blocked the maximal pyloric response to leucine-enkephalin. We concluded intraduodenal mixed amino acids or tryptophan increase phasic, spike-dependent pyloric contractions in the cat via nonvagal, naloxone-sensitive neural pathways, phenylalanine, a structurally similar essential amino acid, had no effect on the feline gastroduodenal junction, and the pyloric responses to exogenous CCK-OP are mediated by pathways distinct from the responses to tryptophan or mixed amino acids.

Effects of magnesium deficiency on duodenal and ileal magnesium absorption and secretion.

Intestinal adaptation by the growing rat to a low-magnesium diet was studied by in situ perfusion of duodenum and ileum in vivo. Rats were fed diets containing either 0.066 or 0.022% Mg for 3 weeks. Magnesium-restricted rats became hypomagnesemic and hypercalcemic. Net magnesium secretion was studied by perfusing an initially magnesium-free saline solution; secretion was higher in duodenum than in ileum, and decreased significantly in the duodenum in response to magnesium restriction. Net magnesium adsorption studied by intraluminal perfusion of 2.5 mM magnesium in saline was greater in duodenum than ileum in rats taking a low-magnesium diet, but duodenal and ileal absorption did not differ in animals taking the normal magnesium diet. Absorption did not adapt significantly to magnesium restriction in either segment. Adaptation of small-intestinal magnesium transport to a low magnesium diet is minimal, consisting mainly of reduced duodenal magnesium secretion.

Altered Pancreatic Function After Proximal Gastric Vagotomy in Man

The secretion of bicarbonate into the duodenum in response to stepwise increasing doses of secretin (0.078, 0.23, 0.7, and 2.1 U/kg-hr) was investigated in 11 duodenal ulcer patients before and about 1 1/2 years after proximal gastric vagotomy. After the vagotomy the mean output of bicarbonate in response to the two lowest doses of secretin increased from 2.2 to 3.7 mmoles per 30 min im response to 0.078 U/kg-hr and from 6.6 to 9.8 mmoles per 30 min in response to 0.23 U/kg-hr. On the other hand, the output of bicarbonate in response to the highest dose of secretin decreased from 20.3 mmoles per 30 min before to 16.5 mmoles per 30 min after the vagotomy. The dose of secretin required for half-maximal stimulation decreased from 0.7 to 0.3 U/kg-hr. The calculated maximal bicarbonate response decreased from 27.8 to 17.7 mmoles per 30 min. Thus, increased sensitivity of the bicarbonate-producing cells to low doses of secretin and decreased bicarbonate secretory capacity of the pancreas after proximal gastric vagotomy were found.

Duodenal and ileal adaptation to dietary calcium restriction: in vivo studies in the rat.

Intestinal adaptation by the growing rat to a low-calcium diet was studied by in situ perfusion of duodenum and ileum in vivo. Rats were fed diets containing either 1.2 or 0.02% Ca for 17-24 days. To study plasma-to-lumen flux and net calcium absorption, rats were loaded parenterally with 45Ca and perfused intraluminally with 3.4 mM calcium. Calcium restriction caused net absorption in ileum to increase fourfold, in duodenum almost twofold. With calcium restriction, plasma-to-lumen flux decreased in duodenum but not in ileum and was small relative to absorption. However, net calcium secretion, when measured in a separate set of animals by intraluminal perfusion of NaCl, decreased in ileum but not in duodenum in response to calcium restriction. The magnitude of adaptation is greater in ileum than duodenum and is largely the result of increased lumen-to-plasma flux. The distal small intestine is probably crucial for calcium homeostasis in dietary calcium deficiency.

Trypsin and chymotrypsin in duodenal aspirate and faeces in response to secretin and cholecystokinin-pancreozymin.

The secretion of trypsin and chymotrypsin into the duodenum in response to secretin and CCK-PZ has been compared with the faecal excretion of the enzymes following similar stimulation in 47 individuals undergoing clinical investigation. The faecal output of chymotrypsin correlated well, but trypsin less satisfactorily, with the secretion of the respective enzymes into the duodenum. The faecal excretion of chymotrypsin following stimulation with secretin and CCK-PZ can therefore be used as an index of pancreatic enzyme-secretory capacity.

Further studies of the response to secretin and pancreozymin in man.

A comparison has been made of the patterns of secretion of bicarbonate, trypsin, and bile pigment into the human duodenum in response to various dose rates of secretin alone and in combination with pancreozymin. Pancreozymin increased the output of bicarbonate to levels greater than achieved with secretin alone. High dose rates of secretin delayed and lowered the pancreozymin-induced pancreatic secretion of enzymes and discharge of bile pigment into the duodenum. The different patterns of response to changing absolute and proportional amounts of stimulant hormones must be taken into account when pancreatic exocrine secretory capacity is to be measured.

Secretory response to secretin in a patient with diarrhoea and the Zollinger-Ellison pattern of gastric secretion.

In a woman with diarrhoea and the Zollinger-Ellison pattern of gastric secretion, the secretion of fluid and bicarbonate into the duodenum in response to secretin was found to be significantly greater than in controls. No pancreatic tumour was found at operation. The pancreas was, however, larger than normal. The patient did not show symptoms of peptic ulcer disease until vagotomy and pyloroplasty had been performed. A capacity to secrete large amounts of bicarbonate was believed to be the explanation of why she was able to tolerate great amounts of acid.

Observations on the Effect of Diversion of Acid from the Duodenum in Response to Gastrin and Histamine

Observations on the Effect of Diversion of Acid from the Duodenum in Response to Gastrin and Histamine

Observations on the effect of diversion of acid from the duodenum in response to gastrin and histamine.

Observations on the effect of diversion of acid from the duodenum in response to gastrin and histamine.

The role of the sphincter of Oddi in the etiology of peptic ulcer. I. Evidence from a review of the literature.

The sphincter of Oddi occupies a key position anatomicaly. Situated as it is at the terminus of the main pancreatic and common bile ducts, it regulates the flow of pancreatic juice and bile into the duodenum in response to a wide variety of stimuli. This important sphincter is subject to many influences, mechanical, chemical, pharmacological, hormonal, and nervous. Its role in the etiology of acute and recurrent pancreatitis has been repeatedly stressed in the literature of the past 30 years, with recent reemphasis on section of the sphincter as an operative maneuver of therapeutic value.* The etiologic relationship of the sphincter of Oddi to biliary dyskinesia, cholecystitis, and the postcholecystectomy syndrome is also mentioned, and, in the recent literature, section of the sphincter of Oddi has been recommended in the last-named condition.† It is the intent of this review to stress in addition the possible critical role of the sphincter