Elevated motility-related transmucosal potential difference in the upper small intestine in the irritable bowel syndrome

被引:37
作者
Larsson, M. H. [1 ]
Simren, M.
Thomas, E. A.
Bornstein, J. C.
Lindstroem, E.
Sjoevall, H.
机构
[1] AstraZeneca R&D, Dept Integrat Pharmacol Gastrointestinal Biol, S-43183 Molndal, Sweden
[2] Univ Gothenburg, Sahlgrenska Acad, Physiol Sect, Dept Neurosci & Physiol, Gothenburg, Sweden
[3] Univ Melbourne, Dept Physiol, Parkville, Vic 3052, Australia
关键词
celiac disease; irritable bowel syndrome; migrating motor complex; secretion; transmucosal potential difference;
D O I
10.1111/j.1365-2982.2007.00941.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
The pathophysiology of irritable bowel syndrome (IBS) is complex and incompletely known. Very little has been studied regarding the role of submucous neuronal activity. We therefore measured small intestinal transmural potential difference (PD, reflecting mainly electrogenic chloride secretion), and its linkage with fasting motor activity [migrating motor complex (MMC)] in controls (n = 16) and patients with IBS [n = 23, 14 diarrhoea predominant (d-IBS) and nine constipation predominant (c-IBS)]. Transmural-PD and its relation to MMC phase III was measured by modified multilumen manometry for 3 h in the fasting state using one jejunal and one duodenal infusion line as flowing electrodes. The amplitude and duration of motor phase III was similar in controls and IBS patients, but the propagation speed of phase III was higher in IBS patients. In IBS patients, maximal PD during MMC phase III was significantly elevated in both the duodenum and jejunum (P < 0.05) and the PD decline after phase III was significantly prolonged in the jejunum (P < 0.01). The PD elevation was seen in both duodenum and jejunum in d-IBS patients, but only in the jejunum in the c-IBS patients. On the basis of previous modelling studies, we propose that the enhanced secretion may reflect disturbed enteric network behaviour in some patients with IBS.
引用
收藏
页码:812 / 820
页数:9
相关论文
共 35 条
[1]   Chloride secretion by the intestinal epithelium: Molecular basis and regulatory aspects [J].
Barrett, KE ;
Keely, SJ .
ANNUAL REVIEW OF PHYSIOLOGY, 2000, 62 :535-572
[2]  
BAXTER PS, 1989, LANCET, V1, P464
[3]   Sensory transmission in the gastrointestinal tract [J].
Blackshaw, L. A. ;
Brookes, S. J. H. ;
Grundy, D. ;
Schemann, M. .
NEUROGASTROENTEROLOGY AND MOTILITY, 2007, 19 :1-19
[4]   Recurrent networks of submucous neurons controlling intestinal secretion:: a modeling study [J].
Chambers, JD ;
Bornstein, JC ;
Sjövall, H ;
Thomas, EA .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2005, 288 (05) :G887-G896
[5]   NEUROIMMUNE SIGNALING IN REGULATION OF INTESTINAL ION-TRANSPORT [J].
COOKE, HJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1994, 266 (02) :G167-G178
[6]   ELECTRICAL POTENTIAL DIFFERENCE AND SODIUM AND POTASSIUM FLUXES ACROSS RECTAL MUCOSA IN ULCERATIVE-COLITIS [J].
EDMONDS, CJ ;
PILCHER, D .
GUT, 1973, 14 (10) :784-789
[8]   Intrinsic primary afferent neurons and nerve circuits within the intestine [J].
Furness, JB ;
Jones, C ;
Nurgali, K ;
Clerc, N .
PROGRESS IN NEUROBIOLOGY, 2004, 72 (02) :143-164
[9]   The spectrum of irritable bowel syndrome: A clinical review [J].
Gilkin, RJ .
CLINICAL THERAPEUTICS, 2005, 27 (11) :1696-1709
[10]   THE RELATIONSHIP BETWEEN GASTROINTESTINAL MOTILITY AND SECRETION [J].
GREENWOOD, B ;
DAVISON, JS .
AMERICAN JOURNAL OF PHYSIOLOGY, 1987, 252 (01) :G1-G7