Relevant bibliographies by topics / Duodenum – Innervation

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Academic literature on the topic 'Duodenum – Innervation'

Author: Grafiati
Published: 4 June 2021
Last updated: 3 February 2022

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Journal articles on the topic "Duodenum – Innervation"

1

Li, Cuiping, Yaohui Zhu, Mohan Shenoy, Reetesh Pai, Liansheng Liu, and Pankaj Jay Pasricha. "Anatomical and functional characterization of a duodeno-pancreatic neural reflex that can induce acute pancreatitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 304, no. 5 (March 1, 2013): G490—G500. http://dx.doi.org/10.1152/ajpgi.00012.2012.

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Neural cross talk between visceral organs may play a role in mediating inflammation and pain remote from the site of the insult. We hypothesized such a cross talk exists between the duodenum and pancreas, and further it induces pancreatitis in response to intraduodenal toxins. A dichotomous spinal innervation serving both the duodenum and pancreas was examined, and splanchnic nerve responses to mechanical stimulation of these organs were detected. This pathway was then excited on the duodenal side by exposure to ethanol followed by luminal mustard oil to activate transient receptor potential subfamily A, member 1 (TRPA1). Ninety minutes later, pancreatic inflammation was examined. Ablation of duodenal afferents by resiniferatoxin (RTX) or blocking TRPA1 by Chembridge (CHEM)-5861528 was used to further investigate the duodeno-pancreatic neural reflex via TRPA1. ∼40% of dorsal root ganglia (DRG) from the spinal cord originated from both duodenum and pancreas via dichotomous peripheral branches; ∼50% splanchnic nerve single units responded to mechanical stimulation of both organs. Ethanol sensitized TRPA1 currents in cultured DRG neurons. Pancreatic edema and myeloperoxidase activity significantly increased after intraduodenal ethanol followed by mustard oil (but not capsaicin) but significantly decreased after ablation of duodenal afferents by using RTX or blocking TRPA1 by CHEM-5861528. We found the existence of a neural cross talk between the duodenum and pancreas that can promote acute pancreatitis in response to intraduodenal chemicals. It also proves a previously unexamined mechanism by which alcohol can induce pancreatitis, which is novel both in terms of the site (duodenum), process (neurogenic), and receptor (TRPA1).
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Zhang, Xueguo, William E. Renehan, and Ronald Fogel. "Vagal innervation of the rat duodenum." Journal of the Autonomic Nervous System 79, no. 1 (February 2000): 8–18. http://dx.doi.org/10.1016/s0165-1838(99)00093-4.

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3

Raybould, H. E., and H. H. Holzer. "Duodenal acid-induced inhibition of gastric motility and emptying in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 265, no. 3 (September 1, 1993): G540—G546. http://dx.doi.org/10.1152/ajpgi.1993.265.3.g540.

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The mechanism by which acid in the duodenum inhibits proximal gastric motor function and delays emptying was investigated in urethan-anesthetized and awake rats. Gastric motility inhibited by duodenal acid (0.2 N HCl) in urethan-anesthetized rats was attenuated by 68 and 54%, respectively, by functional ablation of the vagal or spinal sensory innervation with capsaicin. 5-Hydroxytryptamine3 receptor blockade with zacopride (0.2 mg/kg ip) or cholecystokinin (CCK)-A-type receptor blockade with MK-329 (1 mg/kg ip) had no effect on the motility response to acid. In awake rats with chronically implanted gastric and duodenal cannulas, perfusion of the duodenum with acid (0.1 and 0.2 N HCl) inhibited gastric emptying of a nonnutrient liquid (38 and 59%, respectively). Blockade of CCK-A-type receptors reduced by 30% inhibition of gastric emptying induced by 0.1 N HCl. However, functional ablation of the vagal or spinal sensory innervation, 5-hydroxytryptamine3 receptor blockade, or immunoneutralization of secretin by systemic administration of a polyclonal antibody (no. 7842, 1 ml ip) had no effect on acid-induced (0.1 N HCl) inhibition of gastric emptying. Perfusion of the duodenum with 0.2 N HCl but not 0.1 N HCl inhibited proximal gastric motility in awake rats. These results suggest that 1) a duodenal acid load inhibits gastric emptying in part by a mechanism involving CCK and 2) decreased proximal gastric motility plays a minor role in inhibition of gastric emptying in response to acid.
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4

Holzer, H. H., C. M. Turkelson, T. E. Solomon, and H. E. Raybould. "Intestinal lipid inhibits gastric emptying via CCK and a vagal capsaicin-sensitive afferent pathway in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 267, no. 4 (October 1, 1994): G625—G629. http://dx.doi.org/10.1152/ajpgi.1994.267.4.g625.

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The mechanism by which lipid in the duodenum inhibits gastric emptying was investigated in awake rats fitted with chronic gastric and duodenal cannulas. Perfusion of the duodenum with lipid (Intralipid, 5 and 10%; total amount 50 and 100 mg) caused a significant inhibition (26 and 78%, respectively) of gastric emptying of a nonnutrient liquid (0.9% saline). Functional ablation of the capsaicin-sensitive vagal, but not the spinal, sensory innervation to the upper gastrointestinal tract significantly attenuated by 57% lipid-induced inhibition of gastric emptying. In intact rats, administration of a specific cholecystokinin (CCK)-A receptor antagonist, devazepide, significantly attenuated by 66% the response to lipid. Administration of devazepide in perivagal capsaicin-treated rats did not further reduce the response to lipid. These results suggest that lipid in the duodenum inhibits gastric emptying via a mechanism involving an action of CCK at type A receptors and capsaicin-sensitive vagal afferents.
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5

Berthoud, H. R., N. R. Carlson, and T. L. Powley. "Topography of efferent vagal innervation of the rat gastrointestinal tract." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 1 (January 1, 1991): R200—R207. http://dx.doi.org/10.1152/ajpregu.1991.260.1.r200.

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The gastrointestinal territories innervated by the gastric, celiac, and hepatic abdominal vagi were identified in rats with selective branch vagotomies by means of 1) anterograde tracing with the carbocyanine dye DiI injected into the dorsal motor nucleus and 2) measurement of cervical vagal stimulation-induced motility responses throughout the gut axis. Presence of DiI-labeled vagal terminals in the myenteric plexus and evoked motility responses were well correlated across the sampled gastrointestinal (GI) sites. In animals with only the two gastric branches intact, the entire stomach and the most proximal duodenum showed significant motility responses and were densely innervated, having DiI-labeled vagal terminals in almost every ganglion. The hepatic branch was found to primarily innervate the duodenum, with minor projections to the distal antral stomach and the intestines. The two celiac branches were found to almost exclusively innervate the jejunum, ileum, cecum and entire colon, and, together with the other vagal branches, the duodenum. Therefore, while there is some degree of specific innervation by the abdominal vagal branches of the oral-to-anal gut axis, which could be called "viscerotopic," the considerably overlapping innervation of the duodenum does not satisfy a viscerotopy criterion and needs further functional analysis.
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6

Behrns, K. E., M. G. Sarr, R. B. Hanson, and A. R. Zinsmeister. "Neural control of canine small intestinal motility during nonnutrient infusion." American Journal of Physiology-Gastrointestinal and Liver Physiology 271, no. 3 (September 1, 1996): G423—G432. http://dx.doi.org/10.1152/ajpgi.1996.271.3.g423.

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Our aim was to determine the effect of in situ neural isolation of the jejunoileum (extrinsic denervation and disruption of enteric neural continuity with the duodenum) on the spread of single pressure waves (SPW) and clustered contractions (CC) in response to increasing rates of isolated duodenal and jejunoileal nonnutrient infusions. Ten dogs were prepared with duodenal and jejunal infusion and manometry catheters and a diverting proximal jejunal cannula. Five of the dogs also underwent in situ neural isolation of the entire jejuno- ileum A noncaloric solution was infused at 0-15 ml/min into proximal duodenum or jejunum while manometric data were collected. Alterations in direction, distance, and velocity of spread of SPW and CC with increasing rates of intestinal infusion were analyzed by linear regression of responses to increasing infusion rates. Neural isolation of the jejunoileum did not markedly alter characteristics of duodenal or jejunal SPW or CC under conditions of no intestinal infusion. After neural isolation of jejunoileum, increasing rates of jejunal infusion decreased both the proportion and distance of antegrade spread of SPW in duodenum. These findings suggest that extrinsic innervation to the jejunoileum and enteric neural continuity with the duodenum do not regulate jejunal SPW or CC. Increasing rates of nonnutrient intestinal infusions do not alter local motor patterns in the innervated or neurally isolated jejunum, but after neural isolation of the jejunoileum, these infusions do alter characteristics of duodenal SPW by mechanisms independent of neural pathways.
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7

Holle, G. E., D. Hahn, and W. Forth. "Innervation of pylorus in control of motility and gastric emptying." American Journal of Physiology-Gastrointestinal and Liver Physiology 263, no. 2 (August 1, 1992): G161—G168. http://dx.doi.org/10.1152/ajpgi.1992.263.2.g161.

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The motility index (MI) and contractile frequency were determined for the gastric antrum, pylorus, and duodenum during digestive and interdigestive states in eight dogs before and after resection of the ramus pyloricus nervi vagi (NR) and after selective proximal vagotomy (SPV) subsequent to NR. Neither NR nor subsequent SPV altered the migrating motor complex in the interdigestive state. In the digestive state, NR decreased the MI in the antrum, pylorus, and duodenum. The MI did not further change after SPV subsequent to NR. The cholecystokinin antagonist L364,718 decreased MI in the antrum, pylorus, and duodenum. After NR, L364,718 caused a further reduction in the MI during administration. Gastric emptying was accelerated after NR. SPV subsequent to NR increased gastric emptying further. L364,718, in the absence of NR, accelerated gastric emptying but only during the initial period of emptying. After NR, L364,718 also decreased the time required for emptying of 50 and 100% of the meal. After SPV subsequent to NR, no additional acceleration of emptying occurred.
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8

Khurana, Ramesh K., and J. M. Petras. "Sensory innervation of the canine esophagus, stomach, and duodenum." American Journal of Anatomy 192, no. 3 (November 1991): 293–306. http://dx.doi.org/10.1002/aja.1001920309.

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9

Tomaszewska, O., and J. Kaleczyc. "The distribution and chemical coding of neurons supplying the sphincter of Oddi in mammals." Polish Journal of Veterinary Sciences 16, no. 4 (December 1, 2013): 787–96. http://dx.doi.org/10.2478/pjvs-2013-0113.

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Abstract The major duodenal papilla (papilla of Vater) is an important structure associated with the biliary tract and, in some species, the pancreas. It usually represents a slight elevation on the intestinal mucosa where the dilated junction (ampulla of Vater) of the commmon bile duct and pancreatic duct enters the duodenum. The ampulla is surrounded by a specifically arranged muscle structure called the sphincter of Oddi (SO) which controls the flow of bile and pancreatic fluid. The function of the sphincter is regulated by a complex system that involves many hormonal and neural factors. The literature in the field contains detailed data on the morphology of the SO in a number of mammalian species. However, the comprehensive information about the anatomy and neurochemistry of the innervation of this structure is very limited. The present review article summarizes the current knowledge on the innervation of the SO in mammals. Special emphasis has been put on the localization and chemical coding of neurons contributing to this nerve supply.
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10

Stojanovic, Marija, Lj Scepanovic, D. Mitrovic, V. Scepanovic, T. Stojanovic, M. Stojkovic, S. Ilic, and D. Djuric. "Rat duodenal motility in vitro: Prokinetic effects of DL-homocysteine thiolactone and modulation of nitric oxide mediated inhibition." Archives of Biological Sciences 65, no. 4 (2013): 1323–30. http://dx.doi.org/10.2298/abs1304323s.

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Homocysteine is a significant but modifiable risk factor for vascular diseases. As gastrointestinal smooth musculature is similar to blood vessel muscles, we investigated how elevated homocysteine levels affect nitric oxide-mediated neurotransmission in the gut. There is accumulated evidence that a dysfunction of NO neurons in the myenteric plexus may cause various diseases in the gastrointestinal tract such as achalasia, diabetic gastroparesis and infantile hypertrophic pyloric stenosis. In the present study, we aimed to assess the effects of homocysteine on NO-mediated responses in vitro, and to examine the effects of DL-homocysteine thiolactone on the spontaneous motility of rat duodenum and nitrergic neurotransmission. DL-homocysteine thiolactone concentration of 10 ?mol/L leads to the immediate increase in tone, amplitude and frequency of spontaneous movements in isolated rat duodenum. L-NAME (30 ?mol/L) leads to an increase in basal tone, amplitude and frequency of spontaneous contractions. The relaxations induced by EFS were significantly reduced in duodenal segments incubated in DL-homocysteine thiolactone compared with the control group. EFS-induced relaxations were inhibited by L-NAME in both experimental and control groups. These results suggest that a high level of homocysteine causes an important impairment of non-adrenergic non-cholinergic innervation of the rat duodenum.
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Book chapters on the topic "Duodenum – Innervation"

1

Floch, Martin H. "Innervation of the Stomach and Duodenum." In Netter's Gastroenterology, 100–101. Elsevier, 2010. http://dx.doi.org/10.1016/b978-1-4377-0121-0.50043-x.

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"3.29 Vegetative Innervation von Leber, Gallenblase, Magen, Duodenum, Pancreas und Milz." In Innere Organe, edited by Michael Schünke, Erik Schulte, and Udo Schumacher. Stuttgart: Georg Thieme Verlag, 2015. http://dx.doi.org/10.1055/b-0036-131505.

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