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Anatomy of the Rectum and Anus
Published in Han C. Kuijpers, Colorectal Physiology: Fecal Incontinence, 2019
A. P. Meagher, W. J. Adams, D. Z. Lubowski, D. W. King
The submucosal (Meissner) plexus contains fewer and smaller ganglia than the myenteric plexus. It is a complex plexus, arranged in several layers, and contains interstitial cells of Cajal, resembling fibroblasts, which may have a pacemaker function.3
Pathology—Patient with possible Hirschsprung disease: Case study
Published in Victoria A. Lane, Richard J. Wood, Carlos A. Reck-Burneo, Marc A. Levitt, Pediatric Colorectal and Pelvic Surgery, 2017
Victoria A. Lane, Richard J. Wood, Carlos A. Reck-Burneo, Marc A. Levitt
HD is a congenital condition leading to a lack of ganglion cells in the seromuscular layer (Auerbach plexus) and the submucosa (Meissner plexus) of the bowel. The disease most commonly affects the distal large colon (short segment), but long segment disease, total colonic aganglionosis, and total intestinal aganglionosis also occur. Rectosigmoid 75%–80% of casesSplenic flexure or more proximal 10% of casesTotal colonic aganglionosis: 5% (entire colon + rarely small bowel)
Hirschsprung Disease and Disorders of Intestinal Hypoganglionosis
Published in John F. Pohl, Christopher Jolley, Daniel Gelfond, Pediatric Gastroenterology, 2014
Hirschsprung disease (HD) results from the failure of migration in the enteric nervous system in the distal bowel during fetal development. It is characterized by an absence of ganglion cells in the myenteric (Auerbach) and submucosal (Meissner) plexus of the affected bowel and extends proximally in variable lengths from the internal anal sphincter. Short segment or classic HD is confined to the rectum and sigmoid colon, whereas, long segment HD can affect the entire length of the bowel. Rarely, the disorder can also affect variable lengths of the small bowel.
Pharmacological approaches to treat intestinal pain
Published in Expert Review of Clinical Pharmacology, 2023
Mikolaj Swierczynski, Adam Makaro, Agata Grochowska, Maciej Salaga
Among TRP channels, the TRPV1 (also known as capsaicin receptor) has the best recognized involvement in intestinal pathological conditions and visceral pain, especially in IBD and IBS [91]. TRPV1 is mainly expressed in extrinsic primary afferents of neurons, which are mainly present in submucosal (Meissner) plexus within gastrointestinal tract [92]. Mechanistically, it is a nociceptive ligand-gated ion channel with high permeability to calcium (Ca2+) ions [93], however its functionality also comprises thermal, mechanical, voltage and chemosensivity [94]. Because of the nonselectivity of TRPV1, it can be activated by a variety of stimuli including biochemical ligands (including prostaglandins PGE2, PGI2, proinflammatory cytokines, chemokines, serotonin or histamine) and physicochemical environmental conditions (like temperature over 42°C, acidic environment, osmolarity alternations or voltage) with inflammation-related factors found in both categories.
Disruption of the network between Onuf’s nucleus and myenteric ganglia, and developing Hirschsprung-like disease following spinal subarachnoid haemorrhage: an experimental study
Published in International Journal of Neuroscience, 2019
Ozgur Caglar, Binali Firinci, Mehmet Dumlu Aydin, Erdem Karadeniz, Ali Ahiskalioglu, Sare Altas Sipal, Murat Yigiter, Ahmet Bedii Salman
Figure 1(A) shows spinal cord and location of Onuf’s nucleus, S2 nerve roots, spinal cord and dorsal root ganglions (DRGs), non-apoptotic neurons in Onuf’s nucleus in a normal rabbit. Spinal SAH and spastic AKA, spinal cord with Onuf’s nucleus and ischemic deformed neurons of Onuf’s nucleus in a SAH created rabbit are seen in Figure 1(B). Figure 1(C) shows spinal cord, central canal and location of Onuf’s nucleus in circle, degenerated neurons of Onuf’s nucleus and apoptotic neurons in Onuf’s nucleus in a SAH created rabbit. In Figure 2, macroscopic appearances of the intestine of severely neurodegenerated animal following SAH are shown. Normal histopathological appearances of colonic Auerbach’s plexus along with their magnified forms, villi, and Meissner’s plexus are given in Figure 3(I). Histopathological appearances of colonic Auerbach’s plexus along with their magnified forms, denervated lesioned mucosa (Vv), and degenerated Meissner plexus are shown in Figure 3(II). Figure 4(I) shows same histopathological view after stained aldehyde fuxine. Histopathological appearances of colonic degenerated Auerbach’s plexus along with their magnified forms, denervated lesioned mucosa, and degenerated Meissner’s plexus with aldehyde fuxine of a rabbit with SAH are shown seen in Figure 4(II). Figure 5(I) shows normal histopathological appearances of Auerbach plexus of intestine along with their magnified forms, villi, and Meissner’s plexus with NSE. Figure 5(II) shows degenerated histopathological appearances of colonic Auerbach’s plexus along with their magnified forms, villi, and Meissner’s plexus with S-100. In Figure 6, histopathological view of partial degenerated Auerbach plexus of colon along with their magnified forms, villi, and Meissner’s plexus with NSE are shown.