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Acute Gastric Mucosal Lesions (acute + gastric_mucosal_lesion)
Selected AbstractsAcute Gastric Mucosal Lesions Associated with Cytomegalovirus Infection in an Immunocompetent AdultJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 7 2001Mina Nakagawa No abstract is available for this article. [source] Effects of bathing immediately after birth on early neonatal adaptation and morbidity: A prospective randomized comparative studyPEDIATRICS INTERNATIONAL, Issue 5 2000Yasushi Nako Abstract Objective: Because the risks and benefits of early bathing of newborn infants are not well established, we investigated the effects of bathing immediately after birth on rectal temperature, respiratory rate, heart rate, blood pressure, percutaneous arterial blood oxygen saturation (SpO2) and early neonatal morbidity. Methods: The study was designed as a randomized prospective comparative study in the neonatal care unit of a university hospital. A total of 187 healthy term and near-term newborn infants, who were delivered vaginally without asphyxia, between January and December 1997 were the study subjects. We compared findings in newborns who were bathed 2,5 min after birth (n=95) with those of a control group (n=92) who received dry care instead. Groups were comparable with respect to gestational age, birthweight, male : female ratio, Apgar score and umbilical blood pH. Rectal temperature was measured with an electronic thermometer immediately before the intervention bathing or dry care and at 30 min and 1, 2, 3, 8 and 12 h after birth. Heart rate, respiratory rate, systolic and diastolic blood pressure and SpO2 were measured at 1, 2, 8 and 12 h after birth. The incidence of early neonatal morbidity, including hyperbilirubinemia and gastrointestinal and respiratory problems, was also compared. Results: Rectal temperature changed over time postnatally in both groups (P<0.0001, ANOVA) and there was a significant difference in rectal temperature between groups (P<0.0001, ANOVA). Mean (± SEM) rectal temperature at 30 min after birth (i.e. approximately within 20 min after intervention) was significantly higher in the bathed group than in the control (dry care) group (37.30~0.06 vs 37.00~0.05°C, respectively; P=0.000022). Respiratory rate, heart rate, blood pressure and the ratio of the number of infants with SpO2 90,94% and 95,100% did not differ significantly between the two groups. The incidence of early neonatal morbidity, including vomiting, acute gastric mucosal lesion, polycythemia, need for tube feeding, phototherapy and oxygen therapy, also did not differ between the two groups. Conclusions: Early bathing, minutes after birth, did not appear to adversely affect the adaptation of healthy full-term and near-term newborn infants. [source] Gastroprotection of (-)-,-bisabolol on acute gastric mucosal lesions in mice: the possible involved pharmacological mechanismsFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 1 2010Nayrton Flávio Moura Rocha Abstract (-)-,-Bisabolol is an unsaturated, optically active sesquiterpene alcohol obtained by the direct distillation essential oil from plants such as Vanillosmopsis erythropappa and Matricaria chamomilla. (-)-,-Bisabolol has generated considerable economic interest, since it possesses a delicate floral odor and has been shown to have anti-septic and anti-inflammatory activity. The aim of this work was to evaluate the gastroprotective action of (-)-,-bisabolol on ethanol and indomethacin-induced ulcer models in mice, and further investigate the pharmacological mechanisms involved in this action. The oral administration of (-)-,-bisabolol 100 and 200 mg/kg was able to protect the gastric mucosa from ethanol (0.2 mL/animal p.o.) and indomethacin-induced ulcer (20 mg/kg p.o.). Administration of l -NAME (10 mg/kg i.p.), glibenclamide (10 mg/kg i.p.) or indomethacin (10 mg/kg p.o.) was not able to revert the gastroprotection promoted by (-)-,-bisabolol 200 mg/kg on the ethanol-induced ulcer. Dosage of gastric reduced glutathione (GSH) levels showed that ethanol and indomethacin reduced the content of non-protein sulfhydryl (NP-SH) groups, while (-)-,-bisabolol significantly decreased the reduction of these levels on ulcer-induced mice, but not in mice without ulcer. In conclusion, gastroprotective effect on ethanol and indomethacin-induced ulcer promoted by (-)-,-bisabolol may be associated with an increase of gastric sulfydryl groups bioavailability leading to a reduction of gastric oxidative injury induced by ethanol and indomethacin. [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] Preventive effect of Shigyaku-san on progression of acute gastric mucosal lesions induced by compound 48/80, a mast cell degranulator, in ratsPHYTOTHERAPY RESEARCH, Issue 4 2006Yoshiji Ohta Abstract The study examined whether Shigyaku-san (Si-Ni-San) extract (TJ-35), a traditional Kampo medicine, prevents acute gastric mucosal lesion progression in rats treated once with compound 48/80 (C48/80). Rats treated with C48/80 (0.75 mg/kg body weight, i.p.) received TJ-35 (0.15, 0.35 or 0.75 g/kg body weight, p.o.) 0.5 h after the treatment at which time gastric mucosal lesions appeared. At 0.5 h after C48/80 treatment, the gastric mucosa of the treated rats had increased myeloperoxidase (an index of neutrophil infiltration) and xanthine oxidase activities and thiobarbituric acid reactive substances (an index of lipid peroxidation) content. At 3 h after C48/80 treatment, the gastric mucosa of the treated rats showed progressive lesions and further increases in myeloperoxidase and xanthine oxidase activities and thiobarbituric acid reactive substances content and decreases in vitamin E, ascorbic acid and adherent mucus contents and Se-glutathione peroxidase activity. Post-administered TJ-35 attenuated all these changes found at 3 h after C48/80 treatment dose-dependently. These results indicate that TJ-35 prevents the progression of C48/80-induced acute gastric mucosal lesions in rats possibly by attenuating enhanced neutrophil infiltration, enhanced lipid peroxidation associated with decreased vitamin E and ascorbic acid contents and Se-glutathione peroxidase activity, and destruction of the defensive barrier in the gastric mucosa. Copyright © 2006 John Wiley & Sons, Ltd. [source] | ||||||||||