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Functional neuromuscular impairment in severe intestinal dysmotility
Author(s) -
Gallego Diana,
Malagelada Carolina,
Accarino Anna,
Gori Alessandra,
Malagelada Juan Ramón,
Azpiroz Fernando,
De Giorgio Roberto,
Jimenez Marcel
Publication year - 2018
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/nmo.13458
Subject(s) - neuromuscular transmission , jejunum , ileum , interstitial cell of cajal , medicine , gastroenterology , pathophysiology , migrating motor complex , myenteric plexus , motility , gastrointestinal tract , intestinal pseudo obstruction , biology , duodenum , immunohistochemistry , genetics
Background Chronic intestinal pseudo‐obstruction (CIPO) and enteric dysmotility (ED) are severe intestinal motility disorders usually associated with underlying neuromuscular abnormalities. Objective To evaluate the in vitro neuromuscular function of patients with severe intestinal motility disorders. Methods Full‐thickness intestinal biopsies (16 jejunum and 3 ileum) obtained from patients with CIPO (n = 10) and ED (n = 9) were studied using muscle bath and microelectrode techniques. Control samples (n = 6 ileum and n = 6 jejunum) were used to establish the range of normality. Key Results Fourteen parameters were defined to assess muscle contractility and nerve‐muscle interaction: five to evaluate smooth muscle and interstitial cells of Cajal (ICC) and nine to evaluate inhibitory neuromuscular transmission. For each sample, a parameter was scored 0 if the value was inside the normal range or a value of 1 if it was outside. Patients’ samples (CIPO/ED) had more abnormal parameters than controls ( P < 0.001 for both jejunum and ileum). Functional abnormalities were found to be heterogeneous. The most prevalent abnormality was a decreased purinergic neuromuscular transmission, which was detected in 43.8% of jejunal samples. Conclusions and Inferences Abnormalities of neuromuscular intestinal function are detected in vitro in severe intestinal dysmotility. However, consistent with the heterogeneity of the disease pathophysiology, functional impairment cannot be attributed to a single mechanism. Specifically, defects of purinergic neuromuscular transmission may have an important role in motility disorders of the gastrointestinal tract.