Colonic and jejunal motor disturbances after colonic antigen challenge of sensitized rat.

BACKGROUND & AIMS: Inflammation in the colon may alter motility in the proximal gut and potentiate clinical symptoms. The aim of this study was to characterize the effect of colonic anaphylaxis on local (colonic) and remote (small intestinal) motility and identify the mechanism and mediators involved. METHODS: Rats were sensitized by intraperitoneal injection of 10 microg egg albumin and surgically prepared with electrodes in jejunum and colon and a colostomy tube. Colonic and jejunal myoelectric activity were recorded in fasted animals before and after colonic antigen challenge without and then after pretreatment with specific antagonists. RESULTS: Colonic antigen challenge of sensitized rats was associated with significant (1) increase in colonic myoelectric spike activity, (2) disruption of fasting jejunal motility and initiation of aborally propagating spike complexes, and (3) increase in plasma rat mast cell protease II levels with a decrease in granulated mast cells in colon but not jejunum. The myoelectric disturbance in both colon and jejunum was inhibited significantly by pretreatment with atropine and hexamethonium, doxantrazole, cyclooxygenase, and lipoxygenase inhibitors. Methysergide inhibited only the jejunal disturbance. CONCLUSIONS: Colonic antigen challenge of sensitized animals results in local mast cell activation and the release of mediators that modulate neural pathways to initiate both a local colonic and a remote jejunal myoelectric disturbance.

Luminal factors stimulate intestinal repair during the refeeding of malnourished infant rabbits.

We examined the role of luminal versus systemic factors in promoting intestinal recovery during the refeeding of previously malnourished infant rabbits. Malnutrition was induced by litter expansion at 7 days of age. A 20-cm Thirty-Vella (T-V) loop was created in the intestine of each malnourished and dietary control animal at 21 days of age. Beginning on day 28, controls and one half of the malnourished group (malnourished-refed) were fed chow ad libitum, whereas the remainder of the malnourished group received half the amount of chow given to the malnourished-refed group. On day 35, proximal and distal segments from the intact intestine that remained in continuity as well as segments from the excluded T-V loops were examined. Malnutrition severely reduced mucosal mass and disaccharidase activities in the intact distal intestine. A brief period of refeeding led to a rapid recovery of these parameters. In contrast, the excluded T-V loop segments of the control, malnourished, and malnourished-refed groups all displayed decreased mucosal mass and impaired function to a degree similar to that observed in the intact distal segment from the malnourished group. These results indicate that luminal factors are essential for (i) the maintenance of normal intestinal structure and function in infant rabbits and (ii) the promotion of mucosal repair following nutritional rehabilitation of malnourished animals.

Capsaicin-sensitive vagal stimulation-induced gastric acid secretion in the rat: evidence for cholinergic vagal afferents.

1. The effects of electrical vagal stimulation on frequency-dependent gastric acid secretion were investigated in urethane-anaesthetized rats in vivo. 2. Stimulation at 4, 16 or 32 Hz was performed in rats treated with atropine (1 mg kg-1, i.v.), hexamethonium (10 mg kg-1, i.v. bolus and 1 mg kg-1 min-1, i.v. infusion) or atropine and hexamethonium (doses as above); in some experiments pentagastrin (1.2 micrograms kg-1 h-1, i.v. infusion) was infused prior to stimulation. 3. Maximal acid secretion occurred at 16 Hz. This was significantly reduced but not abolished by atropine or hexamethonium and completely abolished after atropine and hexamethonium. In the presence of pentagastrin, the acid secretory response to 16 Hz stimulation was augmented, atropine or hexamethonium reduced stimulated secretion by about 70%, whereas atropine and hexamethonium completely abolished stimulated secretion. 4. In rats in which the vagus nerve was pretreated with capsaicin 10-14 days before experimentation there was a significant reduction (by about 40%) in stimulated acid secretion at 16 Hz, which was virtually abolished by atropine treatment. After acute treatment of the vagus nerve with capsaicin (at the time of experimentation) maximally stimulated acid secretion was significantly reduced by about 50%. 5. Taken together, these results indicate that capsaicin-sensitive afferent fibres contribute to the acid secretory response induced by electrical vagal stimulation in the rat. Based on pharmacological evidence, the capsaicin-sensitive afferent fibres may be cholinergic, since atropine and hexamethonium totally abolish vagal stimulation-induced acid secretion.