Motility of the Pelvic Colon and Rectum of Normal Persons and Patients With Ulcerative Colitis

Spriggs, Edmund A.; Code, Charles F.; Bargen, J. Arnold; Curtiss, Robert K.; Hightower, Nicholas C.

doi:10.1016/s0016-5085(19)36410-8

Cited by 133 publications

(37 citation statements)

References 6 publications

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“…In this, our results agree with those of previous workers. Adler et al (1941) found activity for more than 50% of the time in the descending colon and Spriggs et al (1951) found activity for 36% of the time in the pelvic colon of fasting subjects. It is interesting that there is agreement with these workers as they used large stimulating balloons to record colonic motility.…”

Section: Discussionmentioning

confidence: 93%

“…It is now generally agreed that only some form of continuous manometry is suitable for accurate quantitative work. Early studies using large balloons and relatively insensitive manometers are suspect because of the physiological and mechanical artefacts produced by large distending balloons (Quigley and Brody, 1950) although some information about colonic motility has been obtained by this method (Adler, Atkinson, and Ivy, 1941;Spriggs, Code, Bargen, Curtiss, and Hightower, 1951).…”

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confidence: 99%

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The motility of the pelvic colon: 1 Motility in normals and in patients with asymptomatic duodenal ulcer

Connell¹

1961

Gut

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Section: Discussionmentioning

confidence: 93%

mentioning

confidence: 99%

The motility of the pelvic colon: 1 Motility in normals and in patients with asymptomatic duodenal ulcer

Connell¹

1961

Gut

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“…Colonic motility is generally reduced in patients with ulcerative colitis (Spriggs, Code, Bargen, Curtiss, and Hightower, 1951 ;Kern, Almy, Abbot, and Bogdonoff, 1951;Bloom, LoPresti, and Farrar, 1968;Jalan, Walker, Prescott, Butterworth, Smith, and Sircus, 1970), while notable features of the condition (Lennard-Jones, Lockhart-Mummery, and Morson, 1968), are the striking shortening of the colon with loss of the haustra which are normally maintained in part by an action of the circular muscle of the colon, which also becomes thickened. The smooth x-ray appearance of the colonic wall at barium enema examination has been explained on this basis, but no biochemical differences have hitherto been demonstrated between diseased and normal muscle which satisfactorily explain these changes.…”

Section: Discussionmentioning

confidence: 99%

Mobilization of tissue kallikrein in inflammatory disease of the colon

Zeitlin¹,

Smith²

1973

Gut

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SUMMARY Colonic tissue was taken at operation from 10 patients with active ulcerative colitis and three patients with uncomplicated diverticular disease but with severe symptoms. Levels of kininogen, kallikrein, and kallikrein precursor were measured in blood-free tissue samples. In normal colon tissue a kininogen occurred in the muscle and none was detected in the mucosa. Kallikrein and its precursor were found in mucosa but not in muscle. In acutely inflamed tissue from ulcerative colitis patients relatively high levels of active kallikrein were detected in the underlying colonic muscle. There was little change in the level of kallikrein in inflamed mucosa or of kininogen in the muscle of these patients. No kallikrein was found in colonic muscle from patients with diverticular disease and the mucosal kallikrein level in these patients was unchanged. The findings suggest a mechanism for the formation of kinins in the wall of the colon which is present in ulcerative colitis but not in diverticular disease.

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“…In the afferent loop syndrome, the overgrowth of bacteria in stagnant bowel contents induces mucosal inflammation, edema, ulceration, and even perforation of the intestine. Previous reports have indicated that inflammation suppresses the phasic contractile activity of the affected intestine in patients with ulcerative colitis, [16][17][18] as well as in animal models. 19 These alterations were accompanied by damage to the ICCs, 11,20 which could be responsible for motility disturbances and smooth muscle dysfunction.…”

Section: Discussionmentioning

confidence: 96%

A decreased number of c- kit -expressing cells in a patient with afferent loop syndrome

Kiyohara

Shinomura

Isozaki

et al. 2003

Journal of Gastroenterology

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Following gastrectomy, stasis in the afferent jejunal loop accompanied by an overgrowth of bacteria leads to a number of clinical symptoms, including the so-called afferent loop syndrome. The disturbances in intestinal motility may be related to stagnation of the intestinal contents in the afferent loop. The pacemaker cells for the basic contractile activity of the intestine are thought to be the interstitial cells of Cajal (ICCs). We and others have reported that ICCs express the c- kit receptor, and that a decreased number of c- kit-expressing ICCs is generally thought to result in disturbed intestinal motility. We report here a patient with postgastrectomy afferent loop syndrome with a decreased number of c- kit-expressing cells in the external muscle layer of the dilated intestine, suggesting damage to the ICCs.

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Motility of the Pelvic Colon and Rectum of Normal Persons and Patients With Ulcerative Colitis

Cited by 133 publications

References 6 publications

The motility of the pelvic colon: 1 Motility in normals and in patients with asymptomatic duodenal ulcer

The motility of the pelvic colon: 1 Motility in normals and in patients with asymptomatic duodenal ulcer

Mobilization of tissue kallikrein in inflammatory disease of the colon

A decreased number of c- kit -expressing cells in a patient with afferent loop syndrome

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