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Mucosal Blood Flow (mucosal + blood_flow)
Selected AbstractsInfluence of Helicobacter pylori infection and cetraxate on gastric mucosal blood flow during healing of endoscopic mucosal resection-induced ulcersJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 11 2001Kyoichi Adachi Abstract Background and Aim: Helicobacter pylori (H. pylori) infection is known to affect the gastric microcirculation, and cetraxate is reported to accelerate gastric ulcer healing, possibly by augmenting gastric mucosal blood flow (MBF). The aim of this study is to clarify the effect of H. pylori infection and cetraxate on MBF during gastric ulcer healing. Methods: Forty-two patients who had undergone endoscopic mucosal resection (EMR) were studied. Mucosal blood flow was measured by the use of a laser Doppler flowmeter in the surrounding mucosa and at the ulcer margin, before, 1 day, 1 week and 4 weeks after EMR. Helicobacter pylori infection was confirmed by the use of bacterial culture and histology. After EMR, patients were randomly assigned to receive 30 mg lansoprazole (u.i.d; L-regimen) or 30 mg lansoprazole (u.i.d.) with 200 mg cetraxate (q.i.d; LC-regimen) for 4 weeks. Results: The MBF ratio (MBF at ulcer margin/MBF in surrounding mucosa) 1 week after EMR was significantly lower than that before or 4 weeks after EMR only in H. pylori -positive patients treated with the L-regimen. No such decrease in MBF was observed after 1 week in H. pylori -positive patients treated with the LC-regimen or in H. pylori -negative patients. Conclusion: A transient decrease in MBF was detected at the ulcer margin during healing of EMR-induced ulcers in H. pylori -infected patients. Cetraxate seemed to prevent this decrease in MBF. [source] Monochloramine impairs mucosal blood flow response and healing of gastric lesions in rats: Relation to capsaicin-sensitive sensory neuronsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 3 2001Koji Takeuchi Abstract Aims: We examined the effects of monochloramine (NH2Cl) on the gastric mucosal blood flow (GMBF) response and the healing of ethanol-induced gastric lesions in rats. Methods: Rats fasted for 18 h were given the 99% ethanol p.o. for induction of gastric lesions, and were fed normally from 1 h later onwards. Monochloramine, at non-ulcerogenic doses (5~20 mmol/L), was given p.o. twice daily for 7 days, starting 2 h after ethanol treatment. Results: Gastric lesions caused by ethanol healed almost completely within 7 days with re-epithelialization. The repeated administration of NH2Cl significantly delayed the healing of ethanol-induced gastric lesions in a dose-dependent manner. The damaged mucosa showed a marked rise in H+ permeability, resulting in luminal acid loss, but this process was accompanied by an increase of mucosal blood flow. Monochloramine did not affect the increased mucosal H+ permeability observed in the stomach after damage by ethanol, but significantly inhibited the mucosal hyperemic response associated with luminal acid loss. Prior exposure of the mucosa to NH2Cl (20 mmol/L) did not affect the gastric hyperemic response caused by mucosal application of misoprostol (a prostaglandin E1 derivative) or NOR-3 (a nitric oxide donor), but totally attenuated the increase of GMBF in response to intragastric capsaicin. Impaired healing and GMBF responses were also observed in rats following chemical ablation of capsaicin-sensitive sensory neurons. Conclusions: These results suggest that NH2Cl impaired the healing of acute gastric mucosal lesions at low concentrations, and this action may be attributable, at least partly, to the impairment of gastric hyperemic response caused by the dysfunction of capsaicin-sensitive sensory neurons. [source] Amitriptyline modifies the visceral hypersensitivity response to acute stress in the irritable bowel syndromeALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 5 2009N. M. THOUA Summary Background, Acute physical stress causes alteration in gut autonomic function and visceral hypersensitivity in patients with irritable bowel syndrome (IBS). We have developed a model to measure this stress response. Aim, To assess whether treatment with a drug effective in treating IBS (amitriptyline) alters the response to acute stress in IBS patients. Methods, Nineteen patients with IBS were given amitriptyline 25,50 mg. Patients underwent physical stress (cold pressor) test at baseline and after 3 months of treatment. Physiological parameters measured were: stress perception; systemic autonomic tone [heart rate (HR) and blood pressure (BP)]; gut specific autonomic innervation [rectal mucosal blood flow (RMBF)] and visceral sensitivity (rectal electrosensitivity). Results, Fourteen of 19 (74%) patients improved symptomatically after 3 months of amitriptyline. Acute stress induced increased perception of stress and systemic autonomic tone and reduced RMBF in symptomatic responders and nonresponders (P > 0.05 for all). All nonresponders but only 3 of 14 responders continued to exhibit stress-induced reduced pain threshold at 3 months (change from baseline ,31% vs. +2%, P < 0.03 respectively). Conclusion, In this open study, amitriptyline appears to decrease stress-induced electrical hypersensitivity; this effect is independent of autonomic tone. The gut response to acute stress deserves further study as a model to study drug efficacy in IBS. [source] The roles of prostaglandin E receptor subtypes in the cytoprotective action of prostaglandin E2 in rat stomachALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2000H. Araki Summary Aim: To investigate the EP receptor subtype involved in the gastroprotective action of prostaglandin (PG) E2 using various EP receptor agonists in rats, and using knockout mice lacking EP1 or EP3 receptors. Methods: Male SD rats and C57BL/6 mice were used after an 18-h fast. Gastric lesions were induced by oral administration of HCl/ethanol (150 m m HCl in 60% ethanol). Rats were given various EP agonists i.v. 10 min before HCl/ethanol: PGE2, sulprostone (EP1/EP3 agonist), butaprost (EP2 agonist), 17-phenyl-,-trinorPGE2 (17-phenylPGE2: EP1 agonist), ONO-NT012 (EP3 agonist) and 11-deoxyPGE1 (EP3/EP4 agonist). In a separate study, the effect of PGE2 on HCl/ethanol lesions was examined in EP1 - and EP3 -receptor knockout mice. Results: Gastric lesions induced by HCl/ethanol were dose dependently prevented by PGE2; this effect was mimicked by sulprostone and 17-phenylPGE2 and was significantly antagonized by ONO-AE-829, an EP1 antagonist. Neither butaprost, ONO-NT012 nor 11-deoxyPGE1 exhibited any protective activity against HCl/ethanol-induced gastric lesions. PGE2 caused an inhibition of gastric motility as well as an increase of mucosal blood flow and mucus secretion, the effects being mimicked by prostanoids activating EP1 receptors, EP2/EP3/EP4 receptors and EP4 receptors, respectively. On the other hand, although HCl/ethanol caused similar damage in both wild-type mice and knockout mice lacking EP1 or EP3 receptors, the cytoprotective action of PGE2 observed in wild-type and EP3 -receptor knockout mice totally disappeared in mice lacking EP1 receptors. Conclusion: The gastric cytoprotective action of PGE2 is mediated by activation of EP1 receptors. This effect may be functionally associated with inhibition of gastric motility but not with increased mucosal blood flow or mucus secretion. [source] Role of Vascular Reflex in Nasal Mucosal Swelling in Nasal AllergyTHE LARYNGOSCOPE, Issue 2 2000Tsutomu Numata MD Abstract Objective: In patients with nasal allergy, antigen challenge on the unilateral nasal mucosa results in nasal secretion not only in the ipsilateral but also in the contralateral nasal cavities that can be inhibited almost completely by premedication with atropine sulfate. The present study was performed to elucidate if centrally mediated vascular reflex induced by antigen challenge plays a role in nasal mucosal swelling in subjects with nasal allergy. Methods: Variations of mucosal swelling and mucosal blood flow in the ipsilateral and the contralateral nasal cavities after unilateral antigen challenge were evaluated by acoustic rhinometry and laser Doppler flowmetry in 20 patients with perennial nasal allergy. Results: Unilateral antigen challenge caused ipsilateral and contralateral nasal mucosal swelling in 17 and 13 patients, respectively. Incidence of contralateral nasal mucosal swelling after unilateral antigen challenge was significantly higher compared with that after control disc challenge (P < .001). In 10 patients in whom unilateral antigen challenge caused bilateral nasal mucosal swelling, significant swelling of the nasal mucosa lasted for more than 30 minutes in the ipsilateral nasal cavity after antigen challenge compared with only 15 minutes in the contralateral nasal cavity. Peak values of contralateral mucosal swelling were 45.3% of those of ipsilateral nasal mucosa. Conclusions: Centrally mediated vascular reflex is partially involved in the onset of nasal mucosal swelling observed after antigen challenge in subjects with nasal allergy. However, nasal mucosal swelling that persists and proceeds even 20 minutes after antigen challenge is caused by the direct effects of chemical mediators on the nasal vasculature. [source] Immediate effect of benzalkonium chloride in decongestant nasal spray on the human nasal mucosal temperatureCLINICAL OTOLARYNGOLOGY, Issue 4 2004J. Lindemann Benzalkonium chloride is a preservative commonly used in nasal decongestant sprays. It has been suggested that benzalkonium chloride may be harmful to the nasal mucosa. Decongestion with the vasoconstrictor xylometazoline containing benzalkonium chloride has been shown to cause a significant reduction of the nasal mucosal temperature. The purpose of the present study was to determine the short-term influence of xylometazoline nasal spray with and without benzalkonium chloride on the nasal mucosal temperature. Healthy volunteers (30) were included in the study. Fifteen volunteers received xylometazoline nasal spray (1.0 mg/mL) containing benzalkonium chloride (0.1 mg/mL) and 15 age-matched subjects, received xylometazoline nasal spray without benzalkonium chloride. Using a miniaturized thermocouple the septal mucosal temperature was continuously measured at defined intranasal detection sites before and after application of the nasal spray. The mucosal temperature values did not significantly differ between the group receiving xylometazoline containing benzalkonium chloride and the group receiving xylometazoline spray without benzalkonium chloride before and after decongestion (P > 0.05). In both study groups septal mucosal temperatures significantly decreased after decongestion (P < 0.05) because of a reduction of the nasal mucosal blood flow following vasoconstriction. This study indicates that benzalkonium chloride itself does not seem to influence nasal blood flow and nasal mucosal temperature in topical nasal decongestants. [source] | ||||||||||||||||||||||