Decrease In Gastric Motility Research Articles

Особливості перебігу патології шлунково-кишкового тракту у хворих на гастроезофагеальну рефлюксну хворобу на тлі гіпотиреозу

The article identifies the features of the pathology of the gastrointestinal tract in patients with gastroesophageal reflux disease on the background of hypothyroidism. The frequency of gastroesophageal reflux disease and the severity of this disease increase with age and the presence of comorbid pathology. In the elderly, the frequency of the typical esophageal manifestations decreases, and the erosive esophagitis with atypical symptoms is more common. The growing number of cases of combined thyroid dysfunction with gastropathology requires in-depth study of the reasons for the relationship between these processes. Pathological changes in the gastrointestinal tract in these patients make their condition severer, contributing to the development and progression of metabolic disorders. An important aggravating effect on the regulatory mechanisms of esophageal kinetics has a pathological functioning of the thyroid gland on the background of iodine deficiency. Results and discussion. In patients with gastroesophageal reflux disease with hypothyroidism, all changes in gastric and duodenal function are associated with a decrease in the acid-forming function of the gastric mucosa, due to its atrophy, decreased tone and contractility of the stomach. This in turn leads to a slowing of gastric and duodenal evacuation, dysfunction of the closing capacity of the cardia and, as a consequence, the development of duodenogastroesophageal reflux. The esophageal contents are not so pronounced, so patients with non-erosive forms of esophagitis predominate (46.2%) against 16% of patients in the second group (patients with gastroesophageal reflux disease). At the same time, erosive forms predominate among patients in the control group with predominant acid reflux. It should be noted that there is a clear relationship between the frequency of erosive changes in the esophageal mucosa and the duration of the disease. Thus, among patients of the main group with a 5-year history of the disease, the number of erosive forms of gastroesophageal reflux disease was minimal. The number of erosive changes in the esophageal mucosa increased sharply in patients with a 10-year history and reached its maximum after 15 years from the onset of the disease. Conclusion. The delay in gastric evacuation is more pronounced in patients with gastroesophageal reflux disease on the background of hypothyroidism. It can be explained by a decrease in gastric motility and the presence of duodenostasis. The slowing of gastric evacuation was more pronounced in patients with gastroesophageal reflux disease on the background of reduced thyroid function. In patients with gastroesophageal reflux disease on the background of hypothyroidism there is an alkaline duodenogastroesophageal reflux as a consequence of reduced acid-forming function of the gastric mucosa and reduced contractility of the stomach and duodenum

Medial prefrontal cortex exacerbates gastric dysfunction of rats upon restraint water‑immersion stress.

Restraint water-immersion stress (RWIS) can induce a gastric mucosal lesions within a few hours. The medial prefrontal cortex (mPFC) is involved in the RWIS process. The present study investigated the modulatory effects and molecular mechanisms of the mPFC on gastric function under an RWIS state. Male Wistar rats were divided into four groups; namely, the control, RWIS 4 h (RWIS for 4 h only), sham-operated and bilateral-lesioned (bilateral-lesioned mPFC) groups. The gastric erosion index (EI) and gastric motility (GM) were determined, and the proteomic profiles of the mPFC were assessed by isobaric tags for relative and absolute quantitation (iTRAQ) coupled with two-dimensional liquid chromatography and tandem mass spectrometry. Additionally, iTRAQ results were verified by western blot analysis. Compared with the RWIS 4 h group and the sham-control group, the bilateral-lesioned group exhibited a significantly lower EI (P<0.01). In the bilateral-lesioned group, RWIS led to a significant decrease in EI and GM. When comparing the control and RWIS 4 h groups, 129 dysregulated proteins were identified, of which 88 were upregulated and 41 were downregulated. Gene Ontology functional analysis demonstrated that 29 dysregulated proteins, including postsynaptic density protein 95, were directly associated with axon morphology, axon growth and synaptic plasticity. Ingenuity pathway analysis revealed that the dysregulated proteins were mainly involved in neurological disease signaling pathways, including the NF-κB and ERK signaling pathways. These data indicated that the presence of the mPFC exacerbates gastric mucosal injury in awake rats during RWIS. Although the quantitative proteomic analysis elucidated the nervous system molecular targets associated with the production of gastric mucosal lesions, such as the role of PSD95. The underlying molecular mechanisms of synaptic plasticity need to be further elucidated.

Functional Condition of the Stomach and The Small Bowel after pancreatic resection

Актуальность. На сегодняшний день отсутствует единый подход в выборе наиболее физиологичного способа рекон-структивного этапа операций. Основными методами исследования моторики желудка и тонкой кишки на сегодняшнийдень являются следующие – рентгенологическое исследование желудочно-кишечного тракта с бариевой взвесью, дыха-тельные тесты, а также беспроводные электронные системы.Цель исследования. Определение наиболее физиологичных способов формирования анастомозов при выполнении ради-кального оперативного вмешательства у больных с опухолевым поражением головки поджелудочной железы на основа-нии оценки функционального состояния желудка и тонкой кишки.Материалы и методы. В условиях специализированного отделения хирургии печени и поджелудочной железы ГКБ имС.П. Боткина и отделения методов радионуклеидной диагностики ГКБ №1 им. Н.И. Пирогова проведено проспективноеклиническое исследование функционального состояния желудка и тонкой кишки у больных с опухолевым поражениемголовки поджелудочной железы, которым по показаниям выполнялось радикальное оперативное вмешательство. Боль-ные были разделены на две подгруппы. В первой подгруппе 19 больным была выполнена панкреатогастродуоденальнаярезекция с антрум-резекцией в модификации Child, а во второй, 18 пациентам - пилоросохраняющая панкреатодуоде-нальная резекция – операция Traverso-Longmire. Для исследования моторно-эвакуаторной функции желудка, тонкойкишки и функционирования гепатобилиарной системы применялось одновременное внутривенное и пероральное введениедвух радиофармпрепаратов– технефита и бромезида с последующей регистрацией на двухдетекторной гамма-камере.Оценка состояния билиодигестивных анастомозов выполнялась с помощью внутривенно введенного препарата бромезид,содержащего 120 мегабеккерель (МБк) изотопа технеция Тс-99м, а для оценки гастроэнтероанастомоза применялась10% манная каша, меченая Тс-99м технефитом, с дозой 40 МБк Тс-99м. Исследование движения меченых соединений пожелчным путям и желудочно-кишечному тракту записывалась в память компьютера в течение 120 минут.Результаты и их обсуждение. В группе пациентов после радикального оперативного вмешательства, на предоперацион-ном этапе всем больным было выполнено исследование моторно-эвакуаторной функции верхнего отдела желудочно-ки-шечного тракта: у 21 больного отмечено незначительное замедление пассажа РФП из желудка (до 50 мин.), у 6 - периодполувыведения составил более 80 минут, при норме Т1/2 – 30 мин, что свидетельствовало о нарушении эвакуации пищииз желудка. У 10 пациентов патологии выявлено не было.У всех больных при выполнении второго исследования отмечено замедление выведения РФП из желудка. В первой под-группе период полувыведения РФП из желудка во время второго исследования составил 126,7 мин.±89 мин., что значи-тельно превысило норму (Т1/2 = 30 мин.). При этом замедление эвакуации было обусловлено не столько снижением мото-рики желудка, сколько энтеро-гастральным рефлюксом, преимущественно отмеченным с 90 минуты исследования. Вовремя третьего введения РФП Т1/2 желудка составила 75,3 мин.±17 мин.У пациентов из второй подгруппы, которым была выполнена ППДР, показатели периода полувыведения РФП из желудкабыли следующими: во время второй процедуры - 118,8±44 мин., во время третьей - 46,2±8 мин.Заключение. Применение радионуклеидного способа у больных с опухолевым поражением головки поджелудочной железыпозволяет проводить не только раннюю и комплексную диагностику моторно-эвакуаторной активности желудка, тон-кой кишки, желчных путей, но и более физиологично планировать тот или иной способ оперативного вмешательства.Применение на практике представленной диагностической методики демонстрирует объективные данные наличия убольных, перенесших ПГДР «ложного» гастростаза за счет энтеро-гастрального рефлюкса, а у пациентов, перенесшихППДР - «истинного» гастростаза, обусловленного либо анастомозитом, либо нарушением иннервации стенки выходногоотдела желудка после его мобилизации.Ключевые слова: Опухолевое поражение головки поджелудочной железы, радикальное оперативное вмешательство,гастроэнтероанастомоз, билиодигестивный анастомоз, панкреатогастродуоденальная резекция.

Effect of grouped ST36 or RN12 on gastric motility and sensation

Objective: To investigate the effects of paired ST36 and RN12 acupuncture stimulation on gastric motility and the firing rate of responsible neurons in anesthetized rats. Methods: Using electrophysiological methods, we measured the effects of acupuncture at RN12, ST36, or RN12+ST36 on gastric motility as well as nerve discharges from the gastric sympathetic, vagal nerve, and wide dynamic range (WDR) neurons in the spinal dorsal horn T7-9 in anesthetized rats. Results: 1) Acupuncture at RN12 inhibited gastric motility (83.84±4.49)% and vagal nerve discharge (65.64±5.67)%, but promoted sympathetic nerve activity (243.70±40.67)%; acupuncture at ST36 induced opposing effects on gastric motility (111.31±2.01)% and vagal nerve discharge (166.98±15.92)%. Interestingly, acupuncture at RN12+ST36 together yielded effects similar to that of acupuncture at RN12 alone (93.59±2.05)%, (54.52±7.12)%. 2) WDR neuron discharges induced by gastric distension were inhibited by acupuncture at RN12 (194.56 ± 18.79)%. However, acupuncture at ST36 induced a more significant inhibitory effect. Conclusion: Acupuncture at RN12 inhibits gastric motility by activation of the sympathetic reflex at the spinal level; acupuncture at ST36 promotes gastric motility by activation of the parasympathetic reflex at the supraspinal level, and acupuncture at RN12+ST36 produces a similar decrease in gastric motility as RN12 stimulation alone. Both acupoints decrease the effect of noxious gastric distention on WDR neuron activity, but paired RN12+ST36 stimulation does not significantly affect WDR neuron discharge.

Tu1448 Gabapentin/Pregabalin Improves Symptoms in Patients With Upper GI Functional Disease and Gut Dysmotility

G A A b st ra ct s shown the GI pharmacological effects of allyl isothiocyanate (AITC), a pungent ingredient of wasabi and a TRPA1 channel activator. It was found that 1) AITC impairs tight junction barrier in primary cultures of rat stomachs (Capsaicin 2014, DOI: 10.5772/57289), and 2) no gastric damage by AITC was observed in ex-vivo rat stomachs (Gastroenterology, 138 (5), S-721, 2010). Therefore, this study is to establish a rodent model of impaired gastric motility resulting from gastric low-grade inflammation by AITC, which is reliable produce to evaluate therapeutic agents of FD. METHODS: Gastric low-grade inflammation: Male SD rats were used after 18 h-fasting. Stomachs mounted on ex-vivo chambers under urethaneanesthetized rats treated with omeprazole, were perfused with 50 mM HCl. Vascular permeability (Pontamine Sky blue) was measured during and 90 min after exposure to AITC (0.33~30 mM) for 30 min. A-967079 (10 mM), a TRPA1 channel blocker, was co-applied with AITC. Gastric motility: Male ddY mice were used after 15 h-fasting. Gastric motility was measured by 13C-acetic acid breath test in conscious mice. AITC (1-100 mg/kg, p.o.) was given 30 min before the measurement of motility. Prokinetic agents including itopride (30, 100 mg/kg), mosapride (0.1-1 mg/kg), and neostigmine (30 μg/kg), or a therapeutic agent for FD acotiamide (10, 30 mg/kg) was given s.c. 40 min before the measurement. RESULTS: Gastric low-grade inflammation: AITC increased vascular permeability in exvivo rat stomachs in concentration-dependent manner, which is obviously increased over 10 mM of AITC. However, increased vascular permeability induced by AITC was not inhibited by A-967079. Gastric motility: AITC (%30 mg/kg) impaired gastric motility in dose-dependent manner in conscious mice, those impaired motility was reversible to normal levels for 24 h after treatment of AITC. Decreased gastric motility induced by AITC (80 mg/ kg) was restored by the pretreatment of itopride, mosapride (1 mg/kg), or neostigmine. Acotiamide (100 mg/kg) also recovered decrease of gastric motility. Gastric macroscopic damage was not observed at the end of the experiments and 24 h after treatment of AITC (80 mg/kg). CONCLUSION: These results suggest that AITC induced gastric low-grade inflammation in the rodent stomach, which is independent on TRPA1 channels and no gastric mucosal damage. In addition, AITC produced the impaired gastric motility in conscious mice, whose phenomenon was reversible by prokinetic agents and a therapeutic agent for FD. This rodent model might be useful tool to develop new therapeutic agents for FD.

A New Strategy Using Rikkunshito to Treat Anorexia and Gastrointestinal Dysfunction.

Because the clinical condition of gastrointestinal dysfunction, including functional dyspepsia, involves tangled combinations of pathologies, there are some cases of insufficient curative efficacy. Thus, traditional herbal medicines (Kampo medicines) uniquely developed in Japan are thought to contribute to medical treatment for upper gastrointestinal symptoms. Rikkunshito is a Kampo medicine often used to treat dyspeptic symptoms. Over the past few years, several studies have investigated the efficacy of rikkunshito for dysmotility, for example, upper abdominal complaints, in animals and humans. Rikkunshito ameliorated the decrease in gastric motility and anorexia in cisplatin-treated rats, stress-loaded mice, and selective serotonin reuptake inhibitor-treated rats by enhancing plasma ghrelin levels via serotonin2B/2C receptor antagonism. In addition, rikkunshito ameliorated the decrease in food intake in aged mice and stress-loaded decreased gastric motility via enhanced ghrelin receptor signaling. Several clinical studies revealed that rikkunshito was effective in ameliorating upper gastrointestinal symptoms, including dyspepsia, epigastric pain, and postprandial fullness. In this review, we discuss these studies and propose additional evidence-based research that may promote the clinical use of Kampo medicines, particularly rikkunshito, for treating anorexia and gastrointestinal dysfunction.

Involvements of the lateral hypothalamic area in gastric motility and its regulation by the lateral septum

Ghrelin is an endogenous ligand for the growth hormone secretagogue receptor (GHS-R) pre-dominantly produced in the stomach. Recent studies have shown that it may promote food intake and gastric motility. We aim to explore effects of ghrelin on the gastric distension (GD) sensitive neurons and gastric motility in the lateral hypothalamic area (LHA), and the possible regulation by the lateral septum. Extracellular single unit discharges were recorded and the gastric motility was monitored by administration of ghrelin into LHA and electrical stimulation of lateral septum. Expression of GHS-R was determined by polymerase chain reaction (PCR), western blot and immunohistochemistry staining. Projection of nerve fiber and expression of ghrelin were observed by retrograde tracer and fluo-immunohistochemistry staining. Results revealed that there were GD neurons in the LHA, and administration of ghrelin could excite both GD-excitatory (GD-E) and GD-inhibited (GD-I) neurons in the LHA. The gastric motility was significantly promoted by administration of ghrelin into LHA with a dose dependent manner, which could be completely abolished by treatment with ghrelin receptor antagonist [D-Lys-3]-GHRP-6 or BIM-28163. c-Fos expression was significantly increased after ghrelin administration to the LHA. Electrical stimulation of the lateral septum could significantly excite GD neurons responsive to ghrelin in the LHA as well as promote gastric motility. However, those effects could be absorbed by pre-treatment of [D-Lys-3]-GHRP-6. GHSR-1a expression in the LHA had no change after ghrelin administration to the LHA or electrical stimulating lateral septum. Electrical lesion of the LHA resulted in the decrease of gastric motility. GHS-R and Ghrelin/FG-double labeled neurons were observed in the LHA and lateral septum, respectively. It is suggested that the LHA may involve in promoting gastric motility via ghrelin. The Lateral septum projects to the LHA and exerts some regulating function on the LHA.

Aspiration Prophylaxis and Rapid Sequence Induction for Elective Cesarean Delivery

Aspiration of gastric contents is a rare but feared and potentially fatal complication of anesthesia. In Mendelson’s landmark article on the pathophysiology of pulmonary aspiration in obstetric patients, he recognized that the clinical presentation is different depending on whether the aspirate is solid or liquid. Solid material resulted in suffocation and death, whereas liquid material resulted in “asthma-like” symptoms. Subsequently, he not only demonstrated that lung injury is secondary to gastric acid but also made 2 critical observations: gastric emptying time is delayed during labor, and aspiration occurs when airway reflexes are obtunded by anesthesia. Since 1946, these observations have been considered valid for every parturient who presents for labor and delivery; however, a question arises when caring for the fasted patient who presents for elective cesarean delivery. Does she have the same risk of aspiration as her laboring counterpart? We suggest that she may not be at as high risk as previously thought. This issue emerged when we cared for a primigravida with cardiomyopathy, severe global biventricular hypokinesis, and a left ventricular ejection fraction of 20%. Our decision to proceed with general anesthesia forced us to confront the issue of airway management. Traditional and contemporary teaching considers all obstetric patients to be at increased risk for pulmonary aspiration compared with patients scheduled for nonobstetric elective surgical procedures, mandating pharmacological prophylaxis as well as rapid sequence induction of anesthesia with cricoid pressure. However, the requirements of a patient at risk for aspiration are difficult to reconcile with a judicious, titrated induction of anesthesia that is ideal for a patient with severely compromised cardiac function. Faced with this choice, we opted for a careful induction of anesthesia with mask ventilation before endotracheal intubation, omitting cricoid pressure. This case made us reconsider long-held beliefs about the risk of aspiration in a subset of obstetric patients and specifically ask ourselves whether an appropriately fasted patient presenting for elective cesarean delivery is indeed at increased risk for aspiration compared with patients scheduled for non-obstetric elective procedures. Defining the full stomach has proven difficult. Many investigators have shown that lung injury increases markedly when the pH of the aspirate is 3. The oft-quoted threshold values for defining a full stomach and increased risk of aspiration are gastric volume 0.4 mL/kg with a pH 2.5. These data come from an experiment in a single rhesus monkey in which the investigators directly instilled liquid of varying volumes and acidity into the mainstem bronchus. Lung injury occurred with a volume 0.4 mL/kg and a pH 2.5. This experiment has led to considerable confusion about gastric volume and the risk of aspiration. The authors defined only the amount of aspirate necessary to cause lung injury if the pH was suitably low. The value 0.4 mL/kg has been erroneously interpreted as the amount of gastric volume that puts a patient at risk of aspiration when in fact it is the volume that produced lung injury in a highly contrived laboratory experiment. The more important question is what amount of gastric volume results in regurgitation. Animal data suggest that the residual gastric volume required to produce regurgitation under general anesthesia is much larger than 0.4 mL/kg. As the volume of liquid gastric contents increases, the risk of regurgitation also increases. At some currently unknown volume, this risk may become unacceptably high. There is, however, much evidence showing that if gastric emptying is normal and patients are appropriately fasted, the risk of significant aspiration is extremely low. The critical question to be answered is whether obstetric patients have normal gastric emptying. Mendelson studied laboring patients whom he correctly identified as having delayed gastric emptying. Since then, delayed gastric emptying has frequently been attributed to all obstetric patients. The presumed mechanisms are a hormonally induced decrease in gastric motility and the mechanical and anatomic effect of cephalad displacement of the stomach with distortion of the gastroesophageal From the Department of Anesthesiology, University of Virginia, Charlottesville, Virginia.

Excitation of Melanocortin Receptors in the Dorsal Motor Nucleus of the Vagus (DMV) in the Rat Produces a Marked Decrease in Gastric Motility

Excitation of Melanocortin Receptors in the Dorsal Motor Nucleus of the Vagus (DMV) in the Rat Produces a Marked Decrease in Gastric Motility

Aspiration Prophylaxis and Rapid Sequence Induction for Elective Cesarean Delivery

Aspiration of gastric contents is a rare but feared and potentially fatal complication of anesthesia. In Mendelson’s landmark article on the pathophysiology of pulmonary aspiration in obstetric patients, he recognized that the clinical presentation is different depending on whether the aspirate is solid or liquid. Solid material resulted in suffocation and death, whereas liquid material resulted in “asthma-like” symptoms. Subsequently, he not only demonstrated that lung injury is secondary to gastric acid but also made 2 critical observations: gastric emptying time is delayed during labor, and aspiration occurs when airway reflexes are obtunded by anesthesia. Since 1946, these observations have been considered valid for every parturient who presents for labor and delivery; however, a question arises when caring for the fasted patient who presents for elective cesarean delivery. Does she have the same risk of aspiration as her laboring counterpart? We suggest that she may not be at as high risk as previously thought. This issue emerged when we cared for a primigravida with cardiomyopathy, severe global biventricular hypokinesis, and a left ventricular ejection fraction of 20%. Our decision to proceed with general anesthesia forced us to confront the issue of airway management. Traditional and contemporary teaching considers all obstetric patients to be at increased risk for pulmonary aspiration compared with patients scheduled for nonobstetric elective surgical procedures, mandating pharmacological prophylaxis as well as rapid sequence induction of anesthesia with cricoid pressure. However, the requirements of a patient at risk for aspiration are difficult to reconcile with a judicious, titrated induction of anesthesia that is ideal for a patient with severely compromised cardiac function. Faced with this choice, we opted for a careful induction of anesthesia with mask ventilation before endotracheal intubation, omitting cricoid pressure. This case made us reconsider long-held beliefs about the risk of aspiration in a subset of obstetric patients and specifically ask ourselves whether an appropriately fasted patient presenting for elective cesarean delivery is indeed at increased risk for aspiration compared with patients scheduled for non-obstetric elective procedures. Defining the full stomach has proven difficult. Many investigators have shown that lung injury increases markedly when the pH of the aspirate is 3. The oft-quoted threshold values for defining a full stomach and increased risk of aspiration are gastric volume 0.4 mL/kg with a pH 2.5. These data come from an experiment in a single rhesus monkey in which the investigators directly instilled liquid of varying volumes and acidity into the mainstem bronchus. Lung injury occurred with a volume 0.4 mL/kg and a pH 2.5. This experiment has led to considerable confusion about gastric volume and the risk of aspiration. The authors defined only the amount of aspirate necessary to cause lung injury if the pH was suitably low. The value 0.4 mL/kg has been erroneously interpreted as the amount of gastric volume that puts a patient at risk of aspiration when in fact it is the volume that produced lung injury in a highly contrived laboratory experiment. The more important question is what amount of gastric volume results in regurgitation. Animal data suggest that the residual gastric volume required to produce regurgitation under general anesthesia is much larger than 0.4 mL/kg. As the volume of liquid gastric contents increases, the risk of regurgitation also increases. At some currently unknown volume, this risk may become unacceptably high. There is, however, much evidence showing that if gastric emptying is normal and patients are appropriately fasted, the risk of significant aspiration is extremely low. The critical question to be answered is whether obstetric patients have normal gastric emptying. Mendelson studied laboring patients whom he correctly identified as having delayed gastric emptying. Since then, delayed gastric emptying has frequently been attributed to all obstetric patients. The presumed mechanisms are a hormonally induced decrease in gastric motility and the mechanical and anatomic effect of cephalad displacement of the stomach with distortion of the gastroesophageal From the Department of Anesthesiology, University of Virginia, Charlottesville, Virginia.

Glucose and the vagus: sensory cells savour sweet substances

Glucose and the vagus: sensory cells savour sweet substances

In vitro and in vivo analysis of the effects of corticotropin releasing factor on rat dorsal vagal complex.

In vivo and in vitro electrophysiological experiments were performed on the rat dorsal vagal complex (DVC, i.e. nucleus of the tractus solitarius, NTS, and dorsal motor nucleus of the vagus, DMV) to examine the effects of corticotropin releasing hormone (CRF) on the central components of the vago-vagal reflex control of gastric function. When applied to gastrointestinal projecting DMV neurones, CRF (10-300 nM) induced a concentration-dependent membrane depolarization, an increase in action potential firing rate and decrease in amplitude of the action potential afterhyperpolarization (P < 0.05). Pretreatment with the non-selective CRF antagonist, astressin (0.5-1 microM) or the selective CRF(2) receptor antagonist, astressin 2B (500 nM) attenuated the CRF-induced increase in firing rate but did not alter basal discharge rate. CRF (30-300 nM) increased the amplitude of excitatory postsynaptic currents (EPSCs) evoked by stimulation of the NTS (P < 0.05). An alteration in the paired pulse ratio indicated the EPSC's increase occurred due to actions at presynaptic sites. In the in vivo anaesthetized rat preparation, bilateral microinjections (20 fmol in 20 nl for each site) of CRF in the DVC decreased gastric motility in rats pretreated with the muscarinic agonist, bethanecol (P < 0.05). The effects of CRF were abolished by systemic administration of the NOS inhibitor, L-NAME, or by bilateral vagotomy. We concluded that CRF had both a direct and an indirect excitatory effect on DMV neurones via activation of CRF(2) receptors and the decrease in gastric motility observed following microinjection of CRF in the DVC is due to the activation of an inhibitory non-adrenergic non-cholinergic input to the gastrointestinal tract.

Evaluation of the gastric antiulcerogenic effect of large cardamom (fruits of Amomum subulatum Roxb)

Large cardamom (fruit of Amomum subulatum Roxb, N.O. Zingiberaceae) commonly known as ‘Heel kalan’ or ‘Bari Ilaichi’ is used in Unani system of medicine in gastrointestinal disorders. A crude methanolic extract and its different fractions, viz. essential oil, petroleum ether (60–80°), ethyl acetate and methanolic fractions, were studied in rats for their ability to inhibit the gastric lesions induced by aspirin, ethanol and pylorus ligature. In addition their effects on wall mucus, output of gastric acid and pepsin concentration were recorded. The crude methanolic extract of A. subulatum and its fractions, viz. essential oil, petroleum ether and ethyl acetate, inhibited gastric lesions induced by ethanol significantly, but not those which were induced by pylorus ligation and aspirin. However, ethyl acetate fraction increased the wall mucus in pylorus ligated rats. The results suggest a direct protective effect of ethyl acetate fraction on gastric mucosal barrier. While the observation of decrease in gastric motility by essential oil and petroleum ether fractions suggests the gastroprotective action of the test drug. These investigations validate the use of ‘ Heel kalan’ in gastrointestinal disorders by Unani physicians.

Integration of postprandial function in the proximal gastrointestinal tract. Role of CCK and sensory pathways.

Cholecystokinin (CCK) stimulates vagal afferent fiber discharge, both gastric and intestinal, which seems to result in reflex decrease in gastric motility, gastric acid secretion, and stimulation of pancreatic protein secretion. Endogenous release of CCK by fat or soybean trypsin inhibitor also alters function by way of a capsaicin-sensitive pathway. We suggest that CCK is released locally from the intestine and acts locally or systemically to stimulate vagal afferent fiber discharge to alter proximal gastrointestinal function (Fig. 14). In this way, in addition to its effect on food intake, CCK and the neural pathway integrate function in the proximal gastrointestinal tract, regulating the entry of food into the duodenum to ensure effective digestion and absorption.

G Protein βγ-Subunits Inhibit Purified Adenylate Cyclase Independent of the Activation by Ca2+ and Calmodulin

We investigated the subtype of alpha-adrenoceptors participating in central noradrenergic inhibition of gastric motility in urethane-anesthetized rats. Noradrenaline at 10 nmole administered intracisternally (i.c.) significantly decreased gastric motility. Yohimbine at 10 nmole, i.c., but not the same dose of prazosin, abolished this noradrenaline-induced decrease in gastric motility. Clonidine at 10 nmole, i.c., but not phenylephrine at 20 nmole, significantly decreased gastric motility. These results suggest that alpha 2-adrenoceptor-mediated mechanisms in the brain stem are involved in noradrenergic inhibitory regulation of gastric motility.

Central noradrenergic inhibition of gastric motility in rats

The roles of central noradrenergic mechanisms in the regulation of gastric motility were investigated in urethane-anesthetized rats in whom an intragastric balloon had been placed. Noradrenaline 100 nmol administered intracerebroventricularly (i.c.v.) significantly decreased spontaneous contractions of the stomach and this decrease in gastric motility was not observed in bilaterally vagotomized animals. Intracisternally administered (i.e.) noradrenaline (10 nmol) induced a decrease in gastric motility comparable to that elicited by noradrenaline 100 nmol i.c.v. Phentolamine 10 nmol i.e. but not the same dose of propranolol i.e. significantly antagonized the noradrenaline (10 nmol)-induced inhibition of gastric motility. These results suggest that α-adrenoceptor-mediated noradrenergic mechanisms in the brain stem are involved in the inhibitory regulation of gastric motility.

Involvement of Nicotinic Receptors in the Dorsal Motor Nucleus of the Vagus in Regulation of Gastric Motility in Rats.

Roles of nicotinic receptors in the dorsal motor nucleus of the vagus (DMV) in the regulation of gastric motility were investigated in urethane-anesthetized rats in which an intragastric balloon had been placed. Nicotine (0.1 nmole) microinjected into the DMV but not the nucleus ambiguus induced dual changes, a decrease followed by an increase in gastric motility. Administration of 0.1 nmole of hexamethonium into the DMV significantly inhibited the decrease in gastric motility induced by intravenously administered nicotine.

&lt;b&gt;Contribution of the vagal nerve to a decrease in gastric motility evoked by a portal infusion of D-glucose in rats&lt;/b&gt;&lt;b&gt; &lt;/b&gt;

&lt;b&gt;Contribution of the vagal nerve to a decrease in gastric motility evoked by a portal infusion of D-glucose in rats&lt;/b&gt;&lt;b&gt; &lt;/b&gt;

Involvement of Nicotinic Receptors in the Dorsal Motor Nucleus of the Vagus in Regulation of Gastric Motility in Rats

Rotes of nicotinic receptors in the dorsal motor nucleus of the vagus (DMV) in the regulation of gastric motility were investigated in urethane-anesthetized rats in which an intragastric balloon had been placed. Nicotine (0.1 nmole) microinjected into the DMV but not the nucleus ambiguus induced dual changes, a decrease followed by an increase in gastric motility. Administration of 0.1 nmole of hexamethonium into the DMV significantly inhibited the decrease in gastric motility induced by intravenously administered nicotine.

Central inhibition of gastric motility by intravenously administered nicotine in rats.

Effects of intravenously (i.v.) administered nicotine on gastric motility were investigated in urethane-anesthetized rats in which an intragastric balloon had been placed. I.v. administered nicotine at 75-300 nmole/kg dose-dependently decreased gastric motility. Decrease in gastric motility induced by nicotine at the dose of 300 nmole/kg was inhibited by intracisternally administered hexamethonium. Gastric motility was also decreased by intracisternally applied nicotine (1-10 nmole). These doses were much smaller than those by the intracerebroventricular route in our previous report. Bilateral vagotomy significantly suppressed basal gastric motility. In bilaterally vagotomized animals, nicotine at 1 mumole/kg but not 300 nmole/kg given i.v. significantly decreased the gastric motility maintained at a normal level by electrical stimulation of the vagus nerve. This nicotine-induced decrease in gastric motility, under conditions of electrical stimulation of the vagus nerve, was inhibited by pretreatment with phentolamine. These results suggest that a smaller dose of nicotine given i.v. activates nicotinic receptors in the brainstem and elicits vagally-mediated inhibition of gastric motility. Activation of peripheral alpha-adrenergic mechanisms together with that of central nicotinic mechanisms may be involved in the decreasing effects of a larger dose of nicotine on gastric motility.