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Book Cover
E-book
Author Sarna, Sushil K.

Title Colonic motility : from bench side to bedside / Sushil K. Sarna
Published San Rafael, Calif. (1537 Fourth Street, San Rafael, CA 94901 USA) : Morgan & Claypool, [2010]
©2010
Online access available from:
Colloquium Digital Library of Life Sciences    View Resource Record  

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Description 1 online resource (1 online resource (xiii, 143 pages)) : illustrations, digital file
Series Integrated systems physiology, from molecule to function to disease, 2154-5626 ; # 11
Colloquium series on integrated systems physiology ; # 11
Contents [1]. Introduction -- Motility requirements of different organs -- How gut contractions mix/turn over and propel digesta -- Types of gut contractions -- Rhythmic phasic contractions -- Ultrapropulsive contractions -- Tonic contractions -- Descending inhibition -- Composition of three types of contractions in gut organs -- Functions and spatiotemporal characteristics of colonic contractions -- Colonic rhythmic phasic contractions -- Colonic giant migrating contractions
[2]. Regulatory mechanisms -- Rhythmic phasic contractions -- Short-duration rhythmic phasic contractions -- Excitation-contraction coupling -- Electromechanical coupling -- Pharmacomechanical coupling -- Excitation-inhibition coupling -- Cellular origin and relaxation oscillator characteristics of slow waves -- Regulation of propagation of short-duration RPCs -- Types of enteric neurons and their functional significance -- Motor neurons -- Interneurons -- Intrinsic sensory neurons -- Long-duration RPCs -- Giant migrating contractions -- Tonic contractions -- Excitation-transcription coupling -- Enteric reflexes
[3]. Colonic motility in health -- Methods of recording human colonic motor activity and analysis of data -- Correlation between colonic contractions and propulsion -- Diurnal variations of human colonic motor activity -- Gastrocolonic reflex/response -- Defecation -- What causes random generation of GMCs -- Anorectal motor activity
[4]. Colonic motility dysfunction -- GMCs and visceral pain of gut origin -- Irritable bowel syndrome -- Diarrhea-predominant IBS -- Colonic motor dysfunction in IBS-D patients -- Constipation-predominant IBS, slow-transit constipation, idiopathic constipation, and constipation due to pelvic floor dysfunction -- Colonic motor dysfunction in IBS-C, slow-transit constipation, idiopathic constipation, and pelvic floor dysfunction patients -- Alternating constipation/diarrhea IBS -- Postinfectious IBS -- Cellular and molecular mechanisms of IBS and other types of constipation -- Smooth muscle and enteric neuronal dysfunction -- Impaired gastrocolonic response -- Abdominal cramping/pain -- Stress -- Early-life trauma and IBS -- Impaired enteric reflexes -- Impaired smooth muscle excitation-contraction coupling in slow-transit constipation -- Role of ICCs -- Role of alterations in the expression of neuropeptides in the myenteric plexus and structural damage to enteric neurons and smooth muscle cells -- Epigenetic dysregulation -- Posttransitional histone modifications -- DNA methylation -- Genetics
[5]. Inflammatory bowel disease -- Motility dysfunction in colonic inflammation -- Visceral hypersensitivity in IBD -- Cellular and molecular mechanisms -- Smooth muscle dysfunction -- Enteric neuronal dysfunction -- Diverticular disease -- Colonic motor dysfunction in diverticular disease patients -- Cellular and molecular mechanisms -- References
Summary Three distinct types of contractions perform colonic motility functions. Rhythmic phasic contractions (RPCs) cause slow net distal propulsion with extensive mixing/turning over. Infrequently occurring giant migrating contractions (GMCs) produce mass movements. Tonic contractions aid RPCs in their motor function. The spatiotemporal patterns of these contractions differ markedly. The amplitude and distance of propagation of a GMC are several-fold larger than those of an RPC. The enteric neurons and smooth muscle cells are the core regulators of all three types of contractions. The regulation of contractions by these mechanisms is modifiable by extrinsic factors: CNS, autonomic neurons, hormones, inflammatory mediators, and stress mediators. Only the GMCs produce descending inhibition, which accommodates the large bolus being propelled without increasing muscle tone. The strong compression of the colon wall generates afferent signals that are below nociceptive threshold in healthy subjects. However, these signals become nociceptive; if the amplitudes of GMCs increase, afferent nerves become hypersensitive, or descending inhibition is impaired. The GMCs also provide the force for rapid propulsion of feces and descending inhibition to relax the internal anal sphincter during defecation. The dysregulation of GMCs is a major factor in colonic motility disorders: irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and diverticular disease (DD). Frequent mass movements by GMCs cause diarrhea in diarrhea predominant IBS, IBD, and DD, while a decrease in the frequency of GMCs causes constipation. The GMCs generate the afferent signals for intermittent short-lived episodes of abdominal cramping in these disorders. Epigenetic dysregulation due to adverse events in early life is one of the major factors in generating the symptoms of IBS in adulthood
Analysis Smooth muscle
Slow waves
Enteric neurons
Excitation-contraction coupling
Peristaltic reflex
ICC
Motility disorders
Volume transmission
Synaptic transmission
Irritable bowel syndrome
Inflammatory bowel disease
Diverticular disease
Diarrhea
Constipation
Visceral hypersensitivity
Excitation-inhibition coupling
Descending inhibition
Abdominal pain
Enteric nervous system
Defecation
Notes Series from website
Bibliography Includes bibliographical references (pages 107-143)
Subject Colon (Anatomy) -- Motility.
Colon.
Gastrointestinal Motility.
Form Electronic book
ISBN 9781615041510 (electronic bk.)
1615041516 (electronic bk.)
1615041508
9781615041503
(paperback)