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Butyrate, a by-product of gut bacteria fermentation as well as the digestion of fat in mother's milk, exerts a wide spectrum of beneficial effects in the gastrointestinal tissues. The present study aimed to determine the effects of sodium butyrate on small intestine contractility in neonatal piglets. Piglets were fed milk formula alone (group C) or milk formula supplemented with sodium butyrate (group B). After a 7-day treatment period, isometric recordings of whole-thickness segments of the duodenum and middle jejunum were obtained by electric field stimulation under the influence of increasing doses of Ach (acetylocholine) in the presence of TTX (tetrodotoxin) and atropine. Moreover, structural properties of the intestinal wall were assessed, together with the expression of cholinergic and muscarinic receptors (M1 and M2). In both intestinal segments (duodenum and middle jejunum), EFS (electric field stimulation) impulses resulted in increased contractility and amplitude of contractions in group B compared to group C. Additionally, exposure to dietary butyrate led to a significant increase in tunica muscularis thickness in the duodenum, while mitotic and apoptotic indices were increased in the middle jejunum. The expression of M1 and M2 receptors in the middle jejunum was significantly higher after butyrate treatment. The results indicate increased cholinergic signaling and small intestinal growth and renewal in response to feeding with milk formula enriched with sodium butyrate in neonatal piglets.

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The antihyperglycemic potential of syringaldehyde has been previously investigated; however, the underlying mechanism remains unclear. In this study, we performed a postprandial glucose test (in vivo) including oral glucose tolerance test (OGTT) and oral starch tolerance test (OSTT) in fructose-induced diabetic mice on a high-fat diet for mimicking type 2 diabetes to explore the hypoglycemic efficacy of syringaldehyde and the underlined molecular involvement of syringaldehyde in a glucose-lowering effect. The results revealed that syringaldehyde dose-dependently suppressed blood glucose in both the OSTT and OGTT when referenced to acarbose and metformin, respectively. Surprisingly, syringaldehyde triggered jejunum motility (ex vivo) via activation of the muscarinic-type acetylcholine receptor. By performing virtual screening with molecular docking, the data showed that syringaldehyde nicely interacted with glucagon-like peptide 1 receptor (GLP-1R), peroxisome proliferator-activated receptor (PPAR), dipeptidyl peptidase-IV (DPP-4), acetylcholine M2 receptor, and acetylcholinesterase. These results showed that syringaldehyde can potentiate intestinal contractility to abolish the α-amylase reaction when concurrently reducing retention time and glucose absorption to achieve a glucose-lowering effect in diabetic mice, suggesting its potential therapeutic benefits with improvement for use as a prophylactic and treatment.

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BACKGROUND AND AIM: As means for enhancing gastrointestinal (GI) motility, prokinetics have previously been evaluated in different breeds of horses with varying success. No previous studies were conducted to evaluate the effect of prokinetics on the intestinal tract of Arabian horses breed. Using B-mode ultrasound in the quantification of intestinal contractility, this study aimed to compare the impact of neostigmine and metoclopramide on the intestinal motility of healthy Arabian horses. MATERIALS AND METHODS: Twenty-one clinically healthy Arabian horses were equally distributed into three groups. The control group was administered with 5 mL normal saline intramuscularly (IM). The second group was administered with neostigmine (0.044 mg/kg body weight [BW], IM), and the third group was administered with metoclopramide (0.25 mg/kg BW, IM). Duodenal, cecal, and colonic contractions were counted through ultrasonography for 3 min (pre-administration and 15, 30, 60, 120, and 180 min post-administration). RESULTS: In the neostigmine group, a significant (p<0.05) increase in duodenal, cecal, and colonic contractions was observed 15 min post-administration compared with that in the control group (15±1.0, 11.33±1.53, and 12.33±2.31 vs. 11.0±2.0, 6.33±0.58, and 5.33±0.58 contractions per 3 min, respectively), continuing to 60 min post-administration for the duodenum and cecum and 120 min for colon and then returning to the normal; however, the metoclopramide group showed a significant (p<0.05) increase only in cecal and colonic contractions 60 min post-administration compared with the control group (11.0±1.0 and 12.33±0.58 vs. 6±1.0 and 5.67±0.58 contractions per 3 min, respectively), continuing until the end of the experiment. Excessive sweating, excitation, and straining were recorded following the administration of neostigmine, whereas no side effects were observed in the metoclopramide group. CONCLUSION: Neostigmine improves duodenal, cecal, and colonic contractions in healthy adult Arabian horses, whereas metoclopramide only improves cecal and colonic contractions. Metoclopramide appears to be safer and longer acting than neostigmine in the Arabian horse breed. Ultrasonography is a valuable noninvasive tool for the quantification of intestinal contractility. Future studies should consider the use of various dosages of metoclopramide and administration routes and investigate its impact on horses with GI transit disorders and inclusion in colic post-operative care.

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A new Thymus vulgaris L. solid essential oil (SEO) formulation composed of liquid EO linked to solid excipients has been chemically analysed and evaluated for its intestinal spasmolytic and antispastic effects in ex vivo ileum and colon of guinea pig and compared with liquid EO and excipients. Liquid EO and solid linked EO were analysed by original capillary electrochromatography coupled to diode array detection (CEC-DAD) and liquid chromatography-tandem mass spectrometry (LC-MS/MS) methodologies. The main bioactive constituents are thymol and carvacrol, with minor constituents for a total of 12 selected analysed compounds. Liquid EO was the most effective in decreasing basal contractility in ileum and colon; excipients addiction permitted normal contractility pattern in solid linked EO SEO. In ileum and colon, the Thymus vulgaris L. solid formulation exerted the relaxant activity on K+-depolarized intestinal smooth muscle as well as liquid EO. The solid essential oil exhibits antimicrobial activity against different strains (Staphylococcus aureus, Streptococcus pyogenes, Pseudomonas aeruginosa, Escherichia coli, Salmonella Thyphimurium, Candida albicans) similarly to liquid oil, with activity against pathogen, but not commensal strains (Bifidobacterium Breve, Lactobacillus Fermentum) in intestinal homeostasis. Therefore, Thymus vulgaris L. solid essential oil formulation can be proposed as a possible spasmolytic and antispastic tool in medicine.

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Dopamine (DA) acts as gut motility modulator, via D1- and D2-like receptors, but its effective role is far from being clear. Since alterations of the dopaminergic system could lead to gastrointestinal dysfunctions, a characterization of the enteric dopaminergic system is mandatory. In this study, we investigated the role of DA and D1- and D2-like receptors in the contractility of the circular muscle of mouse distal colon by organ-bath technique. DA caused relaxation in carbachol-precontracted circular muscle strips, sensitive to domperidone, D2-like receptor antagonist, and mimicked by bromocriptine, D2-like receptor agonist. 7-Chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride (SCH-23390), D1-like receptor antagonist, neural toxins, L-NAME (nitric oxide (NO) synthase inhibitor), 2'-deoxy-N6-methyl adenosine 3',5'-diphosphate diammonium salt (MRS 2179), purinergic P2Y1 antagonist, or adrenergic antagonists were ineffective. DA also reduced the amplitude of neurally evoked cholinergic contractions. The effect was mimicked by (±)-1-phenyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol hydrobromide (SKF-38393), D1-like receptor agonist and antagonized by SCH-23390, MRS 2179, or L-NAME. Western blotting analysis determined the expression of DA receptor proteins in mouse distal colon. Notably, SCH-23390 per se induced an increase in amplitude of spontaneous and neurally evoked cholinergic contractions, unaffected by neural blockers, L-NAME, MRS 2179, muscarinic, adrenergic, or D2-like receptor antagonists. Indeed, SCH-23390-induced effects were antagonized by an adenylyl cyclase blocker. In conclusion, DA inhibits colonic motility in mice via D2- and D1-like receptors, the latter reducing acetylcholine release from enteric neurons, involving nitrergic and purinergic systems. Whether constitutively active D1-like receptors, linked to adenylyl cyclase pathway, are involved in a tonic inhibitory control of colonic contractility is questioned.

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BACKGROUND AND OBJECTIVES: Serious functional and structural alterations of gastrointestinal tract are observed in failure of blood supply, leading to gastrointestinal dismotility. Activation of opioid receptors provides cardioprotective effect against ischemia-reperfusion (I/R) injury. The aim of the present study was to determine whether or not remifentanil could reduce I/R injury of small intestine. METHODS: Male Wistar Albino rats were subjected to mesenteric ischemia (30 min) followed by reperfusion (3 h). Four groups were designed: sham control; remifentanil alone; I/R control; and remifentanil + I/R. Animals in remifentanil + I/R group were subjected to infusion of remifentanil (2 ug kg-1 min-1) for 60 min, half of which started before inducing ischemia. Collecting the ileum tissues, evaluation of damage was based on contractile responses to carbachol, levels of lipid peroxidation and neutrophil infiltration, and observation of histopathological features in intestinal tissue. RESULTS: Following reperfusion, a significant decrease in carbachol-induced contractile response, a remarkable increase in both lipid peroxidation and neutrophil infiltration, and a significant injury in mucosa were observed. An average contractile response of remifentanil + I/R group was significantly different from that of the I/R group. Lipid peroxidation and neutrophil infiltration were also significantly suppressed by the treatment. The tissue samples of the I/R group were grade 4 in histopathological evaluation. In remifentanil + I/R group, on the other hand, the mucosal damage was moderate, staging as grade 1. CONCLUSIONS: The pretreatment with remifentanil can attenuate the intestinal I/R injury at a remarkable degree possibly by lowering lipid peroxidation and leukocyte infiltration.

JUSTIFICATIVA E OBJETIVOS: Alterações funcionais e estruturais sérias do trato gastrointestinal são observadas na insuficiência de irrigação sanguínea, levando a alterações da motilidade gastrointestinal. A ativação dos receptores opioides proporciona um efeito cardioprotetor contra a lesão de isquemia/reperfusão (I/R). O objetivo do presente estudo foi determinar se remifentanil pode ou não reduzir a lesão de I/R do intestino delgado. MÉTODOS: Ratos machos albinos, da linhagem Wistar, foram submetidos à isquemia mesentérica (30 minutos) seguida de reperfusão (3 horas). Quatro grupos foram designados: sham controle; remifentanil isolado; controle I/R; remifentanil + I/R. Os animais do grupo remifentanil + I/R foram submetidos à infusão de remifentanil (2 µg kg-1 min-1) por 60 min, metade dos quais iniciou antes da indução da isquemia. Coletando os tecidos do íleo, a avaliação dos danos foi baseada nas respostas contráteis ao carbacol, nos níveis de peroxidação lipídica e infiltração de neutrófilos e na observação das características histopatológicas no tecido intestinal. RESULTADOS: Após a reperfusão, uma diminuição significativa da resposta contrátil induzida por carbacol, um notável aumento tanto da peroxidação lipídica quanto da infiltração de neutrófilos e uma lesão significativa da mucosa foram observados. A média da resposta contrátil no grupo remifentanil + I/R foi significativamente diferente daquela do grupo I/R. A peroxidação lipídica e a infiltração de neutrófilos também foram significativamente suprimidas pelo tratamento. As amostras de tecido do grupo I/R apresentaram grau 4 na avaliação histopatológica. No grupo remifentanil + I/R, por outro lado, a lesão da mucosa foi moderada, apresentando estadiamento de grau 1. CONCLUSÕES: O pré-tratamento com remifentanil pode atenuar a lesão intestinal de I/R em um grau notável, possivelmente pela redução da peroxidação lipídica e da infiltração leucocitária.

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BACKGROUND AND OBJECTIVES: Serious functional and structural alterations of gastrointestinal tract are observed in failure of blood supply, leading to gastrointestinal dismotility. Activation of opioid receptors provides cardioprotective effect against ischemia-reperfusion (I/R) injury. The aim of the present study was to determine whether or not remifentanil could reduce I/R injury of small intestine. METHODS: Male Wistar Albino rats were subjected to mesenteric ischemia (30 min) followed by reperfusion (3h). Four groups were designed: sham control; remifentanil alone; I/R control; and remifentanil+I/R. Animals in remifentanil+I/R group were subjected to infusion of remifentanil (2 ug kg(-1)min(-1)) for 60 min, half of which started before inducing ischemia. Collecting the ileum tissues, evaluation of damage was based on contractile responses to carbachol, levels of lipid peroxidation and neutrophil infiltration, and observation of histopathological features in intestinal tissue. RESULTS: Following reperfusion, a significant decrease in carbachol-induced contractile response, a remarkable increase in both lipid peroxidation and neutrophil infiltration, and a significant injury in mucosa were observed. An average contractile response of remifentanil+I/R group was significantly different from that of the I/R group. Lipid peroxidation and neutrophil infiltration were also significantly suppressed by the treatment. The tissue samples of the I/R group were grade 4 in histopathological evaluation. In remifentanil+I/R group, on the other hand, the mucosal damage was moderate, staging as grade 1. CONCLUSIONS: The pretreatment with remifentanil can attenuate the intestinal I/R injury at a remarkable degree possibly by lowering lipid peroxidation and leukocyte infiltration.

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BACKGROUND AND OBJECTIVES: Serious functional and structural alterations of gastrointestinal tract are observed in failure of blood supply, leading to gastrointestinal dismotility. Activation of opioid receptors provides cardioprotective effect against ischemia-reperfusion (I/R) injury. The aim of the present study was to determine whether or not remifentanil could reduce I/R injury of small intestine. METHODS: Male Wistar Albino rats were subjected to mesenteric ischemia (30min) followed by reperfusion (3h). Four groups were designed: sham control; remifentanil alone; I/R control; and remifentanil+I/R. Animals in remifentanil+I/R group were subjected to infusion of remifentanil (2ugkg(-1)min(-1)) for 60min, half of which started before inducing ischemia. Collecting the ileum tissues, evaluation of damage was based on contractile responses to carbachol, levels of lipid peroxidation and neutrophil infiltration, and observation of histopathological features in intestinal tissue. RESULTS: Following reperfusion, a significant decrease in carbachol-induced contractile response, a remarkable increase in both lipid peroxidation and neutrophil infiltration, and a significant injury in mucosa were observed. An average contractile response of remifentanil+I/R group was significantly different from that of the I/R group. Lipid peroxidation and neutrophil infiltration were also significantly suppressed by the treatment. The tissue samples of the I/R group were grade 4 in histopathological evaluation. In remifentanil+I/R group, on the other hand, the mucosal damage was moderate, staging as grade 1. CONCLUSIONS: The pretreatment with remifentanil can attenuate the intestinal I/R injury at a remarkable degree possibly by lowering lipid peroxidation and leukocyte infiltration.

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The aim of this study was to analyze whether arginine vasopressin (AVP) may be considered a modulator of intestinal motility. In this view, we evaluated, in vitro, the effects induced by exogenous administration of AVP on the contractility of mouse distal colon, the subtype(s) of receptor(s) activated and the action mechanism. Isometric recordings were performed on longitudinal and circular muscle strips of mouse distal colon. AVP (0.001 nM-100 nM) caused concentration-dependent contractile effects only on the longitudinal muscle, antagonized by the V1 receptor antagonist, V-1880. AVP-induced effect was not modified by tetrodotoxin, atropine and indomethacin. Contractile response to AVP was reduced in Ca(2+)-free solution or in the presence of nifedipine, and it was abolished by depletion of calcium intracellular stores after repetitive addition of carbachol in calcium-free medium with addition of cyclopiazonic acid. U-73122, an inhibitor of the phospholipase C, effectively antagonized AVP effects, whilst it was not affected by an adenylyl cyclase inhibitor. Oxytocin induced an excitatory effect in the longitudinal muscle of distal colon at very high concentrations, effect antagonized by V-1880. The results of this study shown that AVP, via activation of V1 receptors, is able to modulate positively contractile activity of longitudinal muscle of mouse distal colon, independently by enteric nerve activation and prostaglandin synthesis. Contractile response is achieved by increase in cytoplasmatic Ca(2+) concentration via extracellular Ca(2+) influx from L-type Ca(2+) channels and via Ca(2+) release from intracellular stores through phospholipase C pathway. No modulation has been observed on the contractility of the circular muscle.

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BACKGROUND: Intestinal damage causes intestinal dysmotility in gastroschisis. Urinary trypsin inhibitor (UTI) has been shown to prevent intestinal damage in chick embryos with gastroschisis. The effect of intra-amniotic administration of UTI on intestinal motility in gastroschisis has not been investigated. METHODS: Five-day-old fertilized chick embryos were used. Gastroschisis was created through the amniotic cavity without opening the allantoic cavity. There were six groups; control, gastroschisis only, gastroschisis plus meconium and three treatment groups. In the treatment groups, 100 IU/mL, 200 IU/mL and 400 IU/mL UTI were instilled into the amniotic cavity of the gastroschisis plus meconium embryos, respectively. Serosal thickness of the intestines in each group was measured histopathologically. The contractions of the intestines were evaluated by in vitro organ bath technique and the responses were expressed as maximal contraction induced by acetylcholine. RESULTS: The serosal thickness was significantly increased in the gastroschisis plus meconium, 100 IU/mL, 200 IU/mL UTI groups compared to control and gastroschisis only groups. The serosal thickness of the 400 IU/mL UTI group was similar to control and gastroschisis only groups. Contractility of the intestines was diminished in the gastroschisis plus meconium, 100 IU/mL and 200 IU/mL UTI groups. There was no significant difference regarding contractility among control, gastroschisis only and 400 IU/mL UTI groups. CONCLUSION: Intra-amniotic administration of UTI preserves intestinal contractility in chick embryos with gastroschisis. However, preservation of intestinal dysmotility by using UTI in the human gastroschisis cases needs further experimental and clinical trials.

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