Neuropeptides in idiopathic chronic constipation (slow transit constipation)

Sjölund, K.; Fasth, S.; Ekman, Rolf; Hultén, L.; Jiborn, Hans; Nordgren, Svante; Sundler, F.

doi:10.1046/j.1365-2982.1997.d01-46.x

Cited by 96 publications

(72 citation statements)

References 21 publications

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“…The denervation of the gut leads to profound changes in the mucosal peptide concentration (23). Thus, it is quite plausible that the combination of neuropeptide concentration with other factors may be able to inhibit the carcinogenic process, since it is well known that the gut neuroendocrine system is significantly altered in the denervated colon and in megacolon (27)(28)(29)(30).…”

Section: Discussionmentioning

confidence: 99%

Intrinsic denervation of the colon is associated with a decrease of some colonic preneoplastic markers in rats treated with a chemical carcinogen

Vespúcio

Turatti

Modiano

et al. 2008

Braz J Med Biol Res

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Denervation of the colon is protective against the colon cancer; however, the mechanisms involved are unknown. We tested the hypothesis that the denervated colonic mucosa could be less responsive to the action of the chemical carcinogen dimethylhydrazine (DMH). Three groups of 32 male Wistar rats were treated as follows: group 1 (G1) had the colon denervated with 0.3 mL 1.5 mM benzyldimethyltetradecylammonium (benzalkonium chloride, BAC); G2 received a single ip injection of 125 mg/kg DMH; G3 was treated with BAC + the same dose and route of DMH. A control group (Sham, N = 32) did not receive any treatment. Each group was subdivided into four groups according to the sacrifice time (1, 2, 6, and 12 weeks after DMH). Crypt fission index, ß-catenin accumulated crypts, aberrant crypt foci, and cell proliferation were evaluated and analyzed by ANOVA and the Student t-test. G3 animals presented a small number of aberrant crypt foci and low crypt fission index compared to G2 animals after 2 and 12 weeks, respectively. From the second week on, the index of ß-catenin crypt in G3 animals increased slower than in G2 animals. From the 12th week on, G2 animals presented a significant increase in cell proliferation when compared to the other groups. Colonic denervation plays an anticarcinogenic role from early stages of colon cancer development. This finding can be of importance for the study of the role of the enteric nervous system in the carcinogenic process.

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Section: Discussionmentioning

confidence: 99%

Intrinsic denervation of the colon is associated with a decrease of some colonic preneoplastic markers in rats treated with a chemical carcinogen

Vespúcio

Turatti

Modiano

et al. 2008

Braz J Med Biol Res

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“…Other inflammatory processes, such as psoriasis, arthritis, and asthma involve increased substance P immunoreactivity of sensory nerves (Levine et al 1985;Naukkarinen et al 1989;Ollerenshaw et al 1991). Unfortunately, we could not address this question directly in our material because the neurochemical indentification of sensory nerves, i.e., co-localization of substance P and CGRP, does not hold for human gut (Gattuso et al 1996;Sjölund et al 1997). …”

Section: Discussionmentioning

confidence: 99%

Quantitative Comparison of Growth-associated Protein-43 and Substance P in Ulcerative Colitis

Vento

Kiviluoto

Keränen

et al. 2001

J Histochem Cytochem.

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S U M M A R YThe aim of this study was to compare immunoreactivities for substance P with other enteric neuropeptides and GAP-43, a general marker for enteric nerves, in normal human colon and in different stages of ulcerative colitis. Tissue samples from normal colon and regions of ulcerative colitis colon were obtained at surgery and immunostained for substance P, vasoactive intestinal polypeptide (VIP), somatostatin, calcitonin gene-related peptide (CGRP), enkephalin, galanin, GAP-43, and neuron-specific enolase (NSE). Visual examination and semiquantitative analysis revealed a clear increase in the immunoreactivity for substance P in ulcerative colitis, whereas no differences were observed in the distribution of the other peptides. Therefore, quantitative analysis was performed only for substance P immunoreactivity in the lamina propria, circular muscle layer, and myenteric ganglia. In the lamina propria, the score of total intensity of substance P immunoreactivity was 0.55 Ϯ 0.15 (mean Ϯ SEM) in normal colon, 1.30 Ϯ 0.35 ( p ϭ 0.087) in least affected colon, and 2.22 Ϯ 0.28 ( p Ͻ 0.001) in moderately affected colon, whereas no significant differences were observed in immunoreactivities for GAP-43. Similar results were obtained for the mean substance P-or GAP-43-immunoreactive area. In the circular muscle layer, the number, density, total intensity, and perimeter of substance P-and GAP-43-immunoreactive fibers were essentially similar in normal colon, and in mild or moderately affected colon. We conclude that ulcerative colitis does not change the density of gut innervation as a whole. However, the density of substance P-containing nerves is specifically increased, probably due to increased peptide synthesis leading to better visibility of the fibers. U lcerative colitis (UC) is an inflammatory ulcerating process in the mucosa of colon, usually characterized by successive exacerbations and remissions of variable intensity and duration. The precise etiology of UC is unknown. Previous studies have revealed that substance P concentration is increased in inflamed colon mucosa of UC patients (Koch et al. 1987;Goldin et al. 1989). Quantitative histochemical studies indicated that this change is due to increased number of substance P-immunoreactive nerve fibers in the lamina propria (Keränen et al. 1995;Watanabe et al. 1998). It has remained unclear whether UC increases the density of enteric innervation in general and whether the increase in substance P occurs through increased intracellular peptide level, sprouting of nerve fibers, or increased number of ganglion neurons.The growth-associated protein-43 (GAP-43) is expressed by nerve fibers under conditions of embryonic growth and axon regeneration. However, GAP-43 is localized abundantly in the autonomic neurons and nerve fibers even in the mature human intestine (Sharkey et al. 1990;Vento and Soinila 1999). The expression of GAP-43 in mature intestine fits with the idea of plasticity of the enteric nervous system and represents the special nature of enteric ner...

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“…Additionally, delay can occur in patients with no colonic dysmotility [30] . Mechanisms of delay include: dysfunction of the autonomic nervous system, disruption in the ENS [31] , disruptions in the neuroendocrine system [32,33] , and/or colonic myopathy [34,35] . Impaired colonic propulsive activity may represent a major mechanism for colonic dysmotility.…”

Section: Physiology Of Dysmotilitymentioning

confidence: 99%