Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In rats, a secretin (Jorpes) intravenous infusion superimposed on an intracolonic sodium acetate perfusion elicits, with respect to control values, a significant depression of Na+ absorption (0.16 mEq./h-0.00 mEq./h.) and mucus secretion (230-40 mg.). When the hormone is superimposed upon an intracolonic infusion of acetic acid, mucus secretion is also significantly inhibited (790-340 mg.). The influence of secretin on organic anion movement was pH related. At pH values of 7.0, absorption was unchanged (0.34--0.33 mEq./h.), at pH values of 2.9, absorption was significantly reduced (0.67-0.41 mEq./h). The secretin impairment of colonic mucus secretion could influence the transport of watersoluble (Na+) and lipid soluble (acetic acid) substances, probably through changes at the "unstirred layer" level.
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PMID:Does secretin influence rat colonic absorption and secretion? 3 Oct 88

Two dogs were equipped with gastric and duodenal cannulas permitting quantitative collection of pure pancreatic juice. Two series of experiments were performed: 1) collection through a short catheter, length 35 cm, volume 0.3 ml, and internal diameter 1.0 mm, and 2) collection through a long catheter used for duodenoscopic cannulation in man, length 110 cm, volume 1.7 ml, and internal diameter 1.0 mm at the tip and 1.4 mm in the other part of the catheter. After a basal period of 30 min the secretion was stimulated with secretin in the doses 0.1, 0.5, and 2.0 clinical units/kg/h, each dose being infused over a period of 30 min. With the long catheter the dose-response curve for fluid and bicarbonate was shifted to the right. The basal secretion of fluid was depressed 40%; with increasing secretory rates the depression was less pronounced. No significant depression of the bicarbonate concentration was seen. The protein secretion was insignificantly reduced.
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PMID:Depression of exocrine pancreatic secretion by collection through duodenoscopic catheters. 43 35

VIP and secretin were compared in regard to their effects on gastric acid and pepsin secretion induced by pentagastrin histamine or a peptone meal as well as on gastric mucosal blood flow and meal induced serum gastrin level in conscious dogs provided with gastric fistulas and denervated fundic pouches. Both VIP and secretin caused a dose-related stimulation of basal pepsin outputs and inhibition of pentagastrin-induced acid secretion. VIP, like secretin, inhibited pentagastrin and meal-induced gastric acid secretion but in contrast to secretin it caused inhibition of acid response to histamine. Inhibition of acid secretion by VIP or secretin was accompanied by secondary reduction in gastric mucosal blood flow in tests with pentagastrin or histamine and by depression of the serum gastrin level in tests with a peptone meal. This study indicates that in comparison with secretin, VIP has a wider spectrum of inhibition of stimulated gastric secretion and may be considered as one of the enterogastrones released in the small intestine.
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PMID:Comparison of vasoactive intestinal peptide (VIP) and secretin in gastric secretion and mucosal blood flow. 76 58

In 14 duodenal Thomas fistula dogs, four of them alcohol-fed for two years, lidocaine, applied topically to the duodenal pancreatic papilla, inhibited secretin-induced pancreatic secretion probably by interrupting duodenopancreatic reflexes that contribute to the "pancreon's" cholinergic tone. Opposite effects were observed with lidocaine administered against a CCK plus secretin background stimulation of the pancreas. The significant rising of volume and protein output above plateau levels were enhanced by chronic alcohol feeding. Lidocaine infused intravenously did not change secretin-induced pancreatic secretion but raised CCK and secretin evoked plateau secretion levels. Chronic alcoholism enhanced these latter effects. Atropine perfusion superimposed on CCK and secretin stimulation did not prevent but raised the intravenous lidocaine-induced pancreatic secretion changes. It is postulated that the modifications elicited by lidocaine sprayed topically and infused intravenously on CCK plus secretin evoked pancreatic secretion plateau levels are due to depression of an anti-CCK factor secreted by the small intestine mucosa.
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PMID:Evidences for duodenopancreatic reflexes and an anti-CCK factor with lidocaine infused intravenously and sprayed topically on pancreatic papilla in nonalcoholic and alcohol-fed dogs. 79 79

The exocrine pancreatic function was studied in humans by performing a secretin-cholecystokinin test before and after treatment with oxytetracycline or chloramphenicol. In the oxytetracycline-treated patients there was a depression of the amylase and lipase outputs in the duodenal secretion, chymotrypsin decreasing only slightly. After treatment with the two antibiotics the calcium secretion was reduced. The other parameters measured in the duodenal secretion remained essentially unchanged. The enzyme dissociation observed in the present studies is considered to reflect the onset of pancreatic dysfunction due to antibiotic administration. As in the previous animal onset of pancreatic dysfunction due to antibiotic administration. As in the previous animal experiments, the suggested explanation for the changes in enzyme secretion is an inhibition of protein synthesis in the exocrine pancreas due to oxytetracycline and chloramphenicol.
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PMID:Exocrine pancreatic function in man after treatment with oxytetracycline and chloramphenicol. 95 76

The thesis is composed of two parts, the first part is concerned with experiments in rats, the second part confirms the findings in human beings. After administration of oxytetracycline, chloramphenicol and cyclophosphamide, respectively, to rats an approximately dose-dependent decrease in the pancreatic secretion of proteins and enzyme activities was demonstrable in vivo under exogenous stimulation. The exocrine pancreatic function was studied in humans by performing a secretin-pancreocymin test before and after treatment with oxytetracycline or chloramphenicol and before and after massive-dose therapy with cyclophosphamide or combined cytotoxic treatment (as outlined by De Vita). The investigations further included an examination of the exocrine pancreatic function in subjects on maintenance therapy with cyclophosphamide or busulfan and a comparison with the exocrine pancreatic function in a group of controls. In the oxytetracycline-treated humans there was a depression of the amylase and lipase activities in the duodenal secretion. Administration of chloramphenicol produced a decrease in the amylase output only. In the patients on massive-dose or continued therapy with cyclophosphamide the pancreatic function remained essentially unchanged. In contrast, cytotoxic combination treatment resulted in decreased activities of amylase and lipase. After maintenance treatment with busulfan a reduction of the trypsin and amylase activities was detectable. The volume and electrolyte outputs were found to remain essentially unchanged in all investigations. An impairment in enzyme synthesis is suggested as the major cause of the observed changes of pancreatic secretion after antibiotic and cytotoxic treatment.
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PMID:[Behavior of exocrine pancreatic function during treatment with antibiotics and antineoplastic agents]. 99 58

Secrepan (Eisai Co. Tokyo, Japan) was administered to 9 healthy volunteers and 36 patients with non-insulin dependent diabetes mellitus (NIDDM) to clarify the effect of secretin on the pancreatic B-cell, by determining the changes in blood of insulin (IRI). Whereas IRI in healthy subjects showed a monophasic change, reaching a peak (delta IRI = 43 +/- 7.3 microunits/ml, M +/- SE) 5 min after secretin loading and returning to the basal level in 15 min, NIDDM patients on diet therapy (delta IRI = 40.2 +/- 7.6 microunits/ml) showed no significant difference from the control group, but NIDDM patients on sulfonylurea (SU) (15.5 +/- 2.4 microunits/ml) and those on insulin therapy (5.3 +/- 1.4 microunits/ml), both showed a significant depression in responsiveness. Further, the changes in insulin secretion after atropine administration in healthy subjects and the changes in IRI response to Secrepan in vagotomized patients were also determined. As a result, data which preclude the possibility of association of the vagus nerve and cholinergic nerve with the stimulation of insulin secretion by secretin were obtained, and a direct action of secretin on the cell of islets of Langerhans was suggested. The maximum IRI response after a secretin load had a significant positive correlation with the IRI response after a 75-gm GTT and the content of C-peptide immunoreactivity in 24-hour urine. Therefore, insulin response to a secretin load can be useful in assessing endogenous insulin secretion and provides a pertinent clinical guide for the selection of an appropriate therapy for diabetes mellitus.
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PMID:Changes in insulin secretion after secretin administration and the implications in diabetes mellitus. 391 Apr 11

The biliary excretion rates of bile acid, lecithin, and cholesterol were measured in unanesthetized dogs after interruption of enterohepatic circulation and during infusions of sodium taurocholate, sodium glycocholate, sodium dehydrocholate, SC2644 (a bicyclic organic acid with high choleretic potency), and secretin. Both lecithin output and cholesterol output were directly related to bile acid excretion rate. The curves describing these relationships were concave downward. Molar concentration ratios of lecithin-to-bile acid declined gradually from approximately 0.4 to 0.2 as bile acid output increased from approximately 1 to 70 mumoles/min. Cholesterol-to-lecithin molar ratios were highest (0.05-0.15) at very low rates of bile acid excretion, but descended rapidly to a plateau (0.03-0.04) which was constant over the entire range of bile acid excretion rates from 10 to 70 mumoles/min. Similar lipid excretion patterns were observed during glycocholate infusion, but secretin-induced choleresis and dehydrocholate-induced choleresis were unaccompanied by any increments in lecithin or cholesterol excretion and SC2644 (which caused a marked increase in canalicular bile production as measured by erythritol clearance) caused a depression of lipid excretion. The data are consistent with the view that lecithin moves passively from cell membranes to intracanalicular micelles, that transport of cholesterol is coupled to lecithin transport, and that there is also a small amount of independent passive transport of cholesterol from membranes to micelles. A model developed on these assumptions has been shown to behave in a fashion consistent with the entire range of these observations.
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PMID:Biliary excretion of lecithin and cholesterol in the dog. 502 35

The effect of intraduodenal trypsin activity on pancreatic exocrine secretion was studied in conscious Syrian golden hamsters provided with bile-pancreatic fistulae. The secretion (secretory volume, amylase and protein output) was stable during a collection period of 14 h without any duodenal infusions. Infusion into the duodenum of bicarbonate or bile did not affect the secretion. When, however, bile-pancreatic juice or trypsin was administered intraduodenally, a marked depression of amylase and protein output was found. After addition of trypsin inhibitor--in a dose sufficient to eliminate all trypsin activity--to either of the two infusates the secretion was restored to the initial values. In a long-term experiment (10 days) repeated subcutaneous injections of cholecystokinin caused a significant increase of pancreatic protein and amylase content in the hamster. Oral trypsin inhibitor administration for 10 days had similar, although not so pronounced effects. Subcutaneous secretin administration was without effect in this respect. The results show that pancreatic enzyme secretion in the Syrian golden hamster is controlled by a negative feedback regulation exerted by intraluminal trypsin. The findings also suggest that both cholecystokinin and orally administered trypsin inhibitor exert trophic effects on the pancreas.
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PMID:Regulatory effects on the pancreas of intraduodenal pancreatic juice and trypsin in the Syrian golden hamster. 620 95

In eight volunteers the effect of pentagastrin (0.15, 1.0 and 6.0 microgram/kg body weight/h), secretin (0.5 and 1.0 clinical units/kg b.w./h), and cholecystokinin (CCK) (0.5 and 1.0 Ivy dog units/kg b.w./h) on the gastric secretion of pepsin was investigated to ascertain whether interaction occurred. A high intraindividual variation was found, and also a significant washout of pepsin in the initial period after stimulation. Pepsin secretion was stimulated after pentagastrin (50% above basal level) and even more after secretin (75%-200% above basal level), whereas no stimulation but a tendency for depression was seen after CCK. With the doses of gastrointestinal hormones used in this investigation, no interaction between secretin and CCK on gastric secretion of pepsin in man was demonstrated.
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PMID:Effect of Pentagastrin, secretin, and cholecystokinin on gastric secretion of pepsin in man. 679 45


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