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The activity of the upper gastrointestinal tract is periodic. It concerns the gastrointestinal and gallbladder motility, gastrointestinal blood flow, gastric, intestinal, pancreatic and biliary secretions, rate of nutrient absorption, and many other physiological events. Nowadays, the periodic activity of the gastrointestinal tract is considered as a basic physiological pattern in conscious animals and humans. Unfortunately, there are considerable species- and age-related as well as individual differences, therefore experimental protocols should consider first describing the individual periodic pattern in the examined animals. A lot of confusion may appear with data interpretation if the periodic activity is neglected, in particular when low physiological-like doses of test substances are used. For instance, the effect of CCK or VIP administration on the exocrine pancreas may differ from negligible effect to strong one depending of the phase of pancreatic secretion. The action of secretagogues on the gastrointestinal tract will also be discussed in terms of the ultradian and circadian cycles.
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The effect of fundectomy on pancreatic secretion in anaesthetized rats

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The aim of present study was to evaluate the influence of surgical fundectomy and exogenous leptin on the secretion of pancreatic juice in anesthetized rats. In male Wistar rats major part of the gastric fundus was surgically removed, and 60 days afterwards the external jugular vein and the pancreatic-biliary duct were catheterized under general anesthesia. The pancreatic-biliary juice (PBJ) was collected in 15 min intervals without introducing it into the duodenum. Intravenous leptin infusions (0.1, 1.0 and 10 µg/kg body weight) were made every 30 min. The same protocol was used in control non operated rats. The PBJ volume was significantly lower in fundectomized rats as compared to control rats and showed no significant effect to exogenous leptin. The PBJ protein output but not trypsin activity was lower in fundectomized rats as compared to control. Leptin reduced the PBJ protein and trypsin outputs in a dose-related manner in the control and experimental group. The inhibition was, however, more evident in the fundectomized rats. Plasma gastrin was higher in fundectomized rats, while plasma leptin and ghrelin were lower. In conclusion, fundectomy seems to reduce the non stimulated pancreatic secretion and modifies the response to leptin in anesthetized rats.
Pancreatic secretion in rats is regulated by feedback inhibition of cholecystokinin (CCK) release by proteases in the gut lumen, but little is known about the role of gastric acid in this regulation. This study, carried out on conscious rats with large gastric fistulas (GF) and pancreatic fistulas, shows that diversion of pancreatic juice results in the progressive stimulation of pancreatic secretion only in rats with the GF closed. When the GF was kept open, the diversion resulted in only small increment in pancreatic secretion and this was accompanied by progressive increase in gastric acid outputs. Similar amounts of HC1 instilled into the duodenum in rats with the GF open fully reproduced the increase in pancreatic secretion observed after the diversion of pancreatic juice. Pretreatment with omeprazole (15 µmol/kg) to suppress gastric acid secretion or with L-364,718 (5 µmol/kg) to antagonize CCK receptors in the diverted state, resulted in the decline in pancreatic secretion similar to that observed after opening the GF. CCK given s.c. (20-320 pmol/kg) failed to cause any significant rise in the post-diversion pancreatic secretion in rats with the GF closed, but stimulated this secretion dose-dependently when the GF was open. Camostate (6-200 mg/kg) in rats with pancreatic juice returned to the duodenum caused dose-dependent increase in pancreatic secretion, but after opening the GF or after omeprazole this increase was reduced by about 75%. This study provides evidence that gastric acid plays a crucial role in the pancreatic response to diversion of pancreatic juice or inhibition of luminal proteases, and that factors that eliminate gastric acid secretion reduce this response.
Central nervous system affects pancreatic secretion of enzymes however,the neural modulation of acute pancreatitis has not been investigated.Leptin and melatonin have been recently reported to affect the inflammatory response of various tissues.The identification of specific receptors for both peptides in the pancreas suggests that leptin and melatonin could contribute to the pancreatic protection against inflammation.The aim of this study was:1/to compare the effect of intracerebroventricular (i.c.v.)or intraperitoneal (i.p.) administration of leptin or melatonin on the course of caerulein-induced pancreatitis (CIP) in the rat,2/to examine the involvement of sensory nerves (SN)and calcitonin gene-related peptide (CGRP)in pancreatic protection afforded by leptin or melatonin,3/to assess the effect of tested peptides on lipid peroxidation products (MDA +4-HNE)in the pancreas of CIP rats,4/to investigate the influence of leptin or melatonin on nitric oxide (NO)release from isolated pancreatic acini and 5/to determine the effects of caerulein and leptin on leptin receptor gene expression in these acini by RT-PCR.CIP was induced by subcutaneous (s.c.)infusion of caerulein (25 µg/kg)to the conscious rats,confirmed by the significant increases of pancreatic weight and plasma amylase and by histological examination.This was accompanied in marked reduction of pancreatic blood flow and significant rise of MDA +4-HNE in the pancreas.Leptin or melatonin were administered i.p.or i.c.v.30 min prior to the start of CIP.Deactivation of SN was produced by s.c.capsaicin (100 mg/kg).An antagonist of CGRP,CGRP8-37 (100 µg/kg i.p.),was given together with leptin or melatonin to the CIP rats.MDA +4-HNE was measured using LPO commercial kit.NO was determined using the Griess reaction.Pretreatment of CIP rats with i.p.leptin (2 or 10 µg/kg)or melatonin (10 or 50 mg/kg)significantly attenuated the severity of CIP.Similar protective effects were observed following i.c.v.application of leptin (0.4 or 2 µg/rat)but not melatonin (10 or 40 µg/rat)to the CIP rats.Capsaicin deactivation of SN or administration of CGRP8-37 abolished above beneficial effects of leptin on CIP,whereas melatonin-induced protection of pancreas was unaffected.Pretreatment with i.p.melatonin (10 or 50 mg/kg),but not leptin,significantly reduced MDA +4-HNE in the pancreas of CIP rats.Leptin (10–9 -10–6 M)but not melatonin (10–8 -10–5 M)significantly stimulated NO release from isolated pancreatic acini.Leptin receptor gene expression in these acini was significantly increased by caerulein and leptin. We conclude that 1/central or peripheral pretreatment with leptin protects the pancreas against its damage induced by CIP,whereas melatonin exerts its protective effect only when given i.p.,but not following its i.c.v.adminstration,2/activation of leptin receptor in the.pancreatic acini appears to be involved in the beneficial effects of leptin on acute pancreatitis, 3/the protective effects of leptin involve sensory nerves,CGRP and increased generation of NO whereas melatonin-induced protection of the pancreas depends mainly on the antioxidant local effect of this indole,and scavenging of the radical oxygen species in the pancreatic tissue.
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Pancreatic secretion differs according to the genotype of growing pigs

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The objective of this study was to investigate the secretion of pancreatic enzymes and antibacterial activity in weaned pigs of three pure breeds, Pietrain, Duroc and Polish synthetic line 990, to look for eventual differences related to the genotype. Six male pigs of each breed, about 24 kg mean body weight, were equipped with chronic pancreatic duct catheters and duodenal cannulas to assess pure pancreatic juice, and jugular vein catheters for blood withdrawal. Pancreatic juice was collected before and after the morning feeding. Protein output and enzyme activities revealed two distinct profiles: strong manifestation of the prandial phase in Pietrain and line 990 pigs, and weak manifestation in Duroc. The antibacterial activity did not follow the enzyme kinetics, and it was the strongest in pancreatic juice from Pietrain pigs. Postprandial insulinaemia was reduced in the order of: line 990>Pietrain>Duroc. A slight (not significant) tendency towards a reduction of leptin after feeding in synthetic line 990 corresponded with elevated secretion of pancreatic enzymes and plasma insulin. The presented results suggest that the prandial secretion of pancreatic juice differs according to genotype, and the differences may be in part related to release of insulin.
W pracy przedstawiono efekty uzyskane w rezultacie przeprowadzonej różnymi metodami długotrwałej kaniulacji trzustki u świń. Jedna z metod polegała na bezpośredniej kaniulacji przewodu trzustkowego dodatkowego po jego nacięciu, natomiast druga była metodą własną - kaniulę wprowadzano przez brodawkę dwunastniczą mniejszą. W czasie 14-dniowego okresu obserwacji oceniano skuteczność metod określając poziom wydzielania soku trzustkowego w obu grupach, różnice indywidualne wewnątrz grup oraz dynamikę wydzielania w ciągu doby. Korzystniejsze wyniki oraz większą efektywność wydzielania, stwierdzono w grupie zwierząt kaniulowanych poprzez brodawkę dwunastniczą mniejszą.
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Brain-gut axis in pancreatic secretion and appetite control

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The stimulation of exocrine pancreatic secretion that has been attributed by Pavlov exclusively to various reflexes (nervism), was then found that it depend also on numerous enterohormones, especially cholecystokinin (CCK) and secretin, released by duodeno-jejunal mucosa and originally believed to act via an endocrine pathway. Recently, CCK and other enterohormones were found to stimulate the pancreas by excitation of sensory nerves and triggering vago-vagal and entero-pancreatic reflexes. Numerous neurotransmitters and neuropeptides released by enteric nervous system (ENS) of gut and pancreas have been also implicated in the regulation of exocrine pancreas. This article was designed to review the contribution of vagal nerves and entero-hormones, especially CCK and other enterohormones, involved in the control of appetitive behavior such as leptin and ghrelin and pancreatic polypeptide family (peptide YY and neuropeptide Y). Basal secretion shows periodic fluctuations with peals controlled by ENS and by motilin and Ach. Plasma ghrelin, that is considered as hunger hormone, increases under basal conditions, while plasma leptin falls to the lowest level. Postprandial pancreatic secretion, classically divided into cephalic, gastric and intestinal phases, involves predominantly CCK, which under physiological conditions acts almost entirely by activation of vago-vagal reflexes to stimulate the exocrine pancreas, being accompanied by the fall in plasma ghrelin and increase of plasma leptin, reflecting feeding behavior. We conclude that the major role in postprandial pancreatic secretion is played by vagus and gastrin in cephalic and gastric phases and by vagus in conjunction with CCK and secretin in intestinal phase. PP, PYY somatostatin, leptin and ghrelin that affect food intake appear to participate in the feedback control of postprandial pancreatic secretion via hypothalamic centers.
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