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The rise in transmural potential difference (PD) and the fluid secretion induced by 5-hydroxytryptamine (5-HT) were measured in rat small intestine in-vivo. Both cisapride and ketanserin abolished the 5-HT-induced rise in systolic blood pressure mediated by 5-HT2 receptors. Cisapride inhibited the 5-HT-induced increases in the transintestinal PD, but over the same dose range it had no effect on the fluid secretion induced by 5-HT. In contrast, ketanserin caused a dose-dependent reduction in 5-HT-induced fluid secretion at doses that failed to influence the rise in PD. It is concluded that different receptors are responsible for the effects of 5-HT on fluid secretion and electrical activity in the rat small intestine.

There is a paucity of information concerning the metabolism of the small intestine in the presence of bacterial endotoxins. The effect Escherichia coli (055:B5) endotoxin (50 ng/ml) on nitrogen metabolism was studied in isolated rat enterocytes incubated in the presence or absence of glutamine and/or glucose as energy substrates.

Interstitial cells of Cajal (ICCs) were first described as primitive neurons found within organs innervated by autonomie nerves. In the gut, ICCs are juxtaposed among enteric nerve fibers and smooth muscle cells, suggesting they may modulate enteric neurotransmission and affect motility. The recent discovery of neurokinin-1 receptor (NKrl)-like immunoreactivity (ir) on ICCs has strengthened this hypothesis. This study compared the distribution of NKlr-ir to the staining patterns of other reported markers of ICCs including cholera toxin subunit b (CTB), neuron specific enolase (NSE), NADH diaphorase, NADPH diaphorase, nitric oxide synthase (NOS), and vimentin. Albino male rats were anesthetized and whole mount preparations of myenteric plexus-longitudinal muscle with attached circular muscle were dissected. ICCs were stained using multi-label techniques and cells were visualized with a Sarastro 2000 confocal laser scanning microscope equipped with Image Space software.In the small intestine, ICCs associated with circular muscle, but not longitudinal muscle, expressed NKlr-ir.

Background It has been known for several years that nematode-induced enteric inflammation impairs myoelectric and contractile activity, More recently, several studies showed that trinitrobenzene sulfonic acid (TNBS) induced inflammation alters in vitro muscle strip contractility. To our knowledge, the effect of TNBS-induced inflammation on small intestinal motility has not been studied in viva in the rat. Aim: To characterize the changes in small intestinal myoelectric activity caused by TNBS-induced inflammation. Methods: 4 bipolar electrodes were implanted at regular intervals on the antimesenterial side of the proximal jejunum of 13 male Wistar rats (250-350 g). During surgery, we administered intraluminally 30 mg TNBS in 0.25 ml ethanol 40% (n=5), 0.25 ml ethanol 40% (n=4) or 0.25 ml water (n=4). One week later, fasting myoelectric activity was recorded during at least 1 hour. The tracings were analyzed semiautomatically and several parameters concerning phase 3 (P3) and the migrating myoelectric complex (MMC) were examined. Results (mean 4SEM) were compared using ANOVA and Chi-square test. Results: Anaiysis of parameters at a single electrode site

Background An aseptic model of tissue injury (the induction of abscesses by subcutaneous injections of turpentine) was used to examine the proposal that changes in glutamine metabolism lead to structural damage in the epithelium of the small intestine during the systemic response to injury and to investigate the role of dietary glutamine in the maintenance of mucosal structure in the small intestine of control and injured rats. Methods Glutamine-free and glutamine-rich (3.6% glutamine by weight) diets were fed to rats before and during an acute-phase response to injury. Pair-fed groups of animals enabled an independent assessment to be made of the effects of the associated dietary restriction on the mucosal epithelium. Results Adaptive increases in villus height and crypt depth were seen in response to 4 days of feeding of the glutamine diet. Pair-feeding (30% dietary restriction) of either diet induced mucosal atrophy (loss of wet weight and nitrogen) without changes in villus height or crypt depth in the proximal tercile of the small intestine. Systemic injury, however, had no effect on the weight or nitrogen content of the mucosa (relative to pair-feeding). Gross histologic appearance, villus height, and crypt depth were also unchanged by the response to injury. Conclusions The study provided no evidence to support the proposal that alterations in the availability of dietary glutamine during systemic injury (induced by turpentine injections) lead to structural damage to the epithelium.

The influence of preadministration of phenobarbital, benzo[alpha]pyrene, and proadifen hydrochloride on 3-O-methylglucose transfer across the everted rat small intestine was examined. The active and passive components of the sugar transport mechanism were evaluated using phlorizin, a potent inhibitor of active transport of sugars. Pretreatment of the animals with phenobarbital did not alter 3-O-methylglucose transfer characteristics. Pretreatment with intraperitoneally administered benzo[alpha]pyrene increased mucosal to serosal transfer of the sugar low (0.1 mM) sugar concentrations. Enhancement of the active transfer of 3-O-methylglucose by pretreatment with proadifen hydrochloride was noted at low sugar concentrations. The passive transfer of the sugar was reduced after pretreatment with proadifen hydrochloride.