Effect of 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced ileitis on the motor function of non-inflamed rat gastric fundus

During intestinal inflammation, motility disturbances are not restricted to inflamed regions, but, may also occur in remote non-inflamed sites of the gastrointestinal tract, Our aim was to investigate the motor function of th e gastric fundus after the induction of terminal ileitis in the rat. Ileal inflammation was induced by intraluminal installation of 2,4,6-trinitrobenz enesulphonic acid (TNBS) into the ileum. Inflammation was assessed both his tologically and biochemically. Contractions and relaxations of longitudinal muscle strips from the gastric fundus were studied 36 h and 1 week later. During the acute phase of ileal inflammation (36 h), the non-inflamed stoma ch was distended. The contractility of longitudinal muscle strips of the. g astric fundus was decreased due to a post-receptor defect, In addition, non adrenergic noncholinergic (NANC) relaxations were inhibited due. to neurona l dysfunction. Aortic contractility remained normal and the more presence o f food in the stomach did not account for the disturbed neuromuscular funct ion in the gastric fundus. Ablation of extrinsic primary afferent neurones by capsaicin further impaired gastric fundus contractility, Transection and re-anastomosis of the jejunum reversed the effect of TNBS-induced ileitis on the neuromuscular function of the gastric fundus, One week after TNBS, c holinergic neurotransmission was increased in the gastric, fundus. During a cute ileitis, smooth muscle cell contractility and inhibitory NANC neurotra nsmission are inhibited in the non-inflamed gastric fundus. This phenomenon may be mediated by intrinsic connections within the enteric nervous system .