Colon motility

Diverticular disease 3. Increased AEA levels in colon strips from patients with diverticular disease participate in alterations of neural control of colon motility 3. None tested... 

ZITTEL T T, MEILE T, HUGE A, KREIS M E, BECKER H D, JEHLE E c (2001) Preoperative intraluminal application of capsaicin increases postoperative gastric and colonic motility in rats. J Gastrointest Surg. 5 503-13. 

Constipation can be due to primary and secondary causes (Table 18-1). Primary or idiopathic constipation is typified by normal-transit constipation, slow-transit constipation, and dyssynergic defecation. In the normal-transit type, colonic motility is unchanged and patients tend to experience hard stools despite normal movements. In the slow-transit type, motility is decreased leading to infrequent harder, drier stools. In dyssynergic defecation (also known as pelvic floor dysfunction), patients have lost the ability to relax the anal sphincter while coordinating muscle contractions of the pelvic floor. Some causes of secondary constipation are listed in Table 18-1. 

C. R., Colonic motility in man features in normal subjects and in patients with chronic idiopathic constipation, Am. J. Gastroenterol. 1999, 94, 1760-1770. 

Barrow L, Spiller RC, Wilson CG. Pathological influences on colonic motility implications for drug delivery. Adv Drug Del Rev 1991 7 201-218. 

Soffer EE, Scalabrini P, Wingate D. Prolonged ambulant monitoring of human colonic motility. Am J Physiol 1989 257 G601-G606. 

There is a great deal of variability in bowel habits from person to person a normal stool frequency may vary from three stools per week up to three stools per day. Constipation is defined as the infrequent passage of stool. It may be secondary to sluggish colonic motility, in which soft stool is seen throughout the colon, or to difficulties with evacuation in which firm stool is seen primarily in the sigmoid and rectum. 

HT3 receptors in the gastrointestinal tract activate visceral afferent pain sensation via extrinsic sensory neurons from the gut to the spinal cord and central nervous system. Inhibition of afferent gastrointestinal 5-HT3 receptors may inhibit unpleasant visceral afferent sensation, including nausea, bloating, and pain. Blockade of central 5-HT3 receptors also reduces the central response to visceral afferent stimulation. In addition, 5-HT3-receptor blockade on the terminals of enteric cholinergic neurons inhibits colonic motility, especially in the left colon, increasing total colonic transit time. 

These agents increase esophageal peristaltic amplitude, increase lower esophageal sphincter (LES) pressure, and enhance gastric emptying. Cisapride also enhances small bowel and colonic motility. 

Q8 Mr Benjamin has a restricted, low-roughage diet and his colonic motility will be helped by increasing its fruit and vegetable content. It may be possible to... 

Q5 Diverticula are sacs, or pouches, of the mucosa which form in the wall of the colon and bulge through the muscular wall of the intestine, often where arteries penetrate the intestinal wall. Their formation is associated with diets of low fibre content and is thought to be related to abnormal colon motility... 

Diverticula, which are pouches of the mucosa, can form and bulge through the muscular wall of the colon. These pouches may become infected and inflamed (diverticulitis), causing abdominal pain. Development of diverticula is associated with low-fibre diets and is thought to be related to abnormal colonic motility and high intraluminal pressures. The chance of developing diverticula increases with age. 

PYY is a 36-amino-acid peptide originally isolated from porcine upper intestine by Tatemoto et al. (26, 27). It contains an A-terminal tyrosine and a C-terminal tyrosine amide and therefore is named peptide YY. It has a high degree of sequence homology (70%) with neuropeptide Y, and it strongly inhibits pancreatic exocrine secretion and jejunal and colonic motility as well as causes vasoconstriction. 

Barrow, L. Spiller, R.C. Wilson, C.G. Pathological influences on colonic motility—implications for drug delivery. 39. Adv. Drug Delivery Rev. 1991, 7 (1), 201-218. 

Fatal colitis has been reported in naares with foals that were being treated with p.o. erythromycin. Erythromycin may also induce diarrhea because of its prokinetic action. It mimics the effects of the hormone motilin on the enteric nervous system, and subantimicrobial doses stimulate small intestinal, cecal and colonic motility. 

Lyrenas E 1985 Beta adrenergic influence on esophageal and colonic motility in man. Scandinavian Journal of Gastroenterology Supplement 116 1-48 MacAllister C G, Lowrey F, Stebbins M et al 1994... 

Ness T J 1999 Kappa opioid receptor agonists differentially inhibit two classes of rat spinal neurons excited by colorectal distention. Gastroenterology 117 388-394 Nguyen A, Camilleri M, Kost L J et al 1997 SDZ HTF 919 stimulates canine colonic motility and transit in vivo. Journal of Pharmacology and Experimental Therapeutics 280 1270-1276... 

Croci T, Cecchi R, Tarantino A, et al. Inhibition of rat colon motility by stimulation of atypical P-adrenoceptors with new gut-specific agents. Pharmacol Res Commun 1988 20 147-151. 

Walker JK, Gainetdinov RR, Mangel AW, Caron MG, Shetzline MA. 2000. Mice lacking the dopamine transporter display altered regulation of distal colonic motility. Am. J. Physiol. Gastrointest. Liver Physiol. 279 0311-18... 

Di Lorenzo C, Flores C F, Hyman P E (1995). Age related changes in colon motility. / Pediatr 127 593-596. 

No chronic changes in colonic motility were observed in rats orally administered 10 or 40 mg/kg sennosides daily for 23 weeks (Fioramonti et al. 1993). 

The amount of secondary products of neutral steroids and bile acids in feces of patients with ulcerative colitis appears to be reduced as compared to normal subjects (88). Thus bacterial action on steroids is decreased, probably owing to enhanced colonic motility, and may lead to reduced absorption of primary and especially secondary bile acids from the colon. This may explain the absence or low level of lithocholic acid in serum (188,193) of these patients and does not support the concept that lithocholic acid causes the liver damage (212) found frequently in ulcerative colitis. 

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