Impaired capsaicin and neurokinin-evoked colonic motility in inflammatory bowel disease.

摘要: Background:  Inflammatory bowel disease (IBD) is associated with altered sensory and motor function in the human colon. The aim of present study was to compare neuromuscular normal IBD-affected colon vitro, emphasis on inhibitory enteric nerves, neuropeptides stimulation axon collaterals. Methods:  Strips longitudinal circular muscle were prepared following colectomy from six patients intestinal carcinoma (mean age 64.2 ± 4.8 years) IBD (Crohn's disease, n = 3; ulcerative colitis, n = 3: mean 35.8 ± 5.7 years). Responses measured electrical field stimulation, potassium chloride, 1,1-dimethyl-4-phenylpiperazinium iodide, isoprenaline, calcitonin gene-related peptide (CGRP), capsaicin neurokinin (NK)-1 -2 receptor subtype-specific agonists, alone or after precontraction. Results:  NK-1 CGRP receptor-mediated relaxation reduced (by 44%, P < 0.05) 61%, colon, respectively. Maximal NK-2 contraction also significantly decreased both (71%, P < 0.001) (51%, P < 0.01) muscle. Capsaicin evoked precontracted colonic muscle; this diminished 63%, P < 0.001 76%, P < 0.01, respectively). by nerves not altered. Conclusions:  Colonic strips exhibited impaired contraction. Capsaicin-activated smooth deficient These results suggest a discrete effect sensory-motor coupling tachykinin-mediated effects motility.