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Objective:To evaluate the efficacy of bedside gastric ultrasound in guiding enteral nutrition therapy in the patients with spontaneous cerebral hemorrhage.Methods:Sixty-one patients with spontaneous intracerebral hemorrhage in the intensive care unit (ICU) of our hospital, aged 18-60 yr, with the European malnutrition risk screening score in 2002 was ≥ 3, who could not eat orally, were selected.All patients received decompression or aneurysm clipping under general anesthesia.Patients were divided into 2 groups using a random number table method: control group ( n=30) and ultrasound group ( n=31). Nutrient infusion pump was used to infuse standard whole protein formula enteral nutrition continuously through a nasogastric tube.In control group, gastric residual volume, residual traits and bowel sounds were evaluated according to gastric drainage to start or adjust enteral nutrition treatment.In ultrasound group, the antral motility index and gastric residual volume were monitored by the modified antral single section method under ultrasound to start or adjust enteral nutrition treatment.The starting time of enteral nutrition, time to reach the target feeding amount, rate of reaching the target feeding standard within 96 h, interruption of enteral nutrition, duration of hospitalization in ICU, and occurrence of intraperitoneal hypertension, aspiration, diarrhea, gastrointestinal bleeding and new pulmonary infection during enteral nutrition therapy were recorded. Results:Compared with control group, the initiation time of enteral nutrition and time to reach the target feeding amount were significantly shortened, the interruption rate of enteral nutrition was decreased, the rate of reaching the target feeding standard within 96 h was increased, the incidence of aspiration and new pulmonary infection was decreased ( P<0.05), and no significant change was found in the duration of hospitalization in ICU and incidence of intraperitoneal hypertension, diarrhea and upper gastrointestinal bleeding in ultrasound group ( P>0.05). Conclusions:Bedside gastric ultrasound-guided enteral nutrition therapy can improve the therapeutic effect with higher safety in the patients with spontaneous intracerebral hemorrhage.
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Objective To evaluate the protective effects of hydrotalcite,Marzulene-s,selbex,gefarnate,sucralfate and rebamipide against the gastric mucosa lesions induced by ethanol,aspirin,hydrochloric acid or prednisolone in rats.The changes in intercellular space width of gastric epithelial in rats was observed. Methods Four kinds of models were used to observe the protective effects of six agents against the gastric mucosal lesions.① Ethanol model:a total of 84 male Wistar rats were divided into 7 groups with 12 each. The rats in group 1 to 7 were orally received hydrotalcite,Marzulene-S,gefarnate,sucralfate,rebamipide or normal saline for 3 days,respectively.On day 4,the rats were given 1 ml of absolute ethanol.The length of gastric lesion were measured by ulcer index.② Aspirin model:the rats were received 300 mg/kg of aspirin and 0.1 mol/L hydrochloric acid (0.5 ml/100 g).The following procedures were as ①.③ Hydrochloric acid model:the rats were received 1 ml of 0.7 mol/L hydrochloric acid. The following procedures were as ①. ④ Prednisolone model: all groups were administrated with above 6 agents or normal saline for 5 days.During the 2nd-5th day,the rats were subcu aneously injected with prednisolone (250 mg/kg) daily. Rats were killed on 5th day,and the lesions were mcasured by ulcer index.Gastric mucosal tissue of No.1,5 and ]0 rat in the control group and the hydrotalcite group were picked up to measure the intercellular space width using transmission electron microscopy. Results In four kind of models,the ulcer index were significantly lower in rats treated with mucosal protective agents than that in the controls (P＜0.05),expecially in hydrotalcite group (P＜0.01).The width of intercellular space in the hydrotalcite group was significantly narrower than that in controls (P＜0.05).Conclusions All of the mucosal protective agents can be against the gastric mucosal lesion induced by ethanol,hydrochloric acid,aspirin or prednisolone.Among them,the hydrotalcite is even better.The effect of hydrotalcite is further confirmed by observation of intercellular space width.
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Objective: To investigate the effect of the acid inhibitor-Lansoprazole on the distribution of Helicobacter pylori (H.pylori) in stomach. Methods: Biopsy specimens were taken from the duodenal ulcer patients who underwent gastroscopy before and after the treatment of Lansoprazole. The biopsy specimens were taken from the lesser curvature of the antrum and the greater curvature of the corpus respectively. H&E and Warthin-Starry staining were used for detecting the changing of active gastritis and the positive rate of H.pylori. Results: (1)The positive rates of H.pylori before treatment, 4 weeks after treatment and 3 months after treatment, in the lesser curvature of the antrum were 93.02%, 58.14%, and 86.05%, respectively. The positive rate and density of H.pylori 4 weeks after treatment were greatly decreased compared with those before treatment (P
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Objective:To assess the mechanism of exacerbation of colonic damage in rat colitis model induced by trinitrobenzene sulfonic acid(TNBS)treated wi th celecoxib(a selective COX-2 inhibitor).Methods:The rats w ere randomized in to four groups.Group 1 and Group 2 were study groups.Group 3 and Group 4 were control groups.Colitis was induced by intracolonic administration of TNBS(25 g /L)in a vehicle of 50% ethanol(0.25 mL)of study groups.The rats of study gro ups were treated orally,beginning 3 h before induction of colitis and continuin g twice per day thereafter for up to 7 d,with celecoxib(1.25 mg/kg,Group 1)a nd distilled water(1 mL/0.3 kg,Group 2)respectively.In control experiments,the rats of Group 4 were treated orally with celecoxib(1.25 mg/kg)twice per da y for up to 7 d.Group 3 rats were healthy control rats.All the rats that survi ved until the end of the experiment(d 7)were killed and the severity of coloni c inflammation was assessed.The COX-2 protein expression in colon tissues was e xamined by immunohistochemistry.Results:The colonic damage of Group 1 was exac erbated as compared with Group 2.The inflammatory index of colon tissues of Gro up 1(8.5?2.5)was significantly reduced,as compared with Group 2(13.5?1.9,P
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Objective: To study the effect of recombinant human intestinal trefoil factor ( rhITF) on the healing of rat chronic gastric ulcer , protect gastric mucosal and mechanisms are involved. Methods: (1) Acute gastric mucosal injury was induced by ethanol, stress, aspirin and pylorusl ligation. The injury index ,MDA, GMBL,hexosamine (Hex) and acid output were measure. (2) Chronic gastric ulcer was induced in rats by application of 50% glacial acetic acid to the serosa of the glandular stomach. After injury, rats received by rhITF or vehicle orally twice daily for 11 days. On day 12, gastric mucosal blood flow(GMBF)was measured under ether anesthesia. Then the pylorus was ligated for 3 hours and each stomach removed. The gastric acid output, ulcer index, Hex and nitric oxide(NO) content in gastric mucosa, as well as iNOSmRNA in the ulcer bed were determined. Results: (1) rhITF protected gastric mucosa from the acute lesion, and increased Hex content in gastric mucosa. (2) rhITF treatment significantly decreased the ulcer index and gastric acid output, but increased the GMBF, Hex and NO content in comparison with the control groups. In addition, rhITF also stimulated iNOSmRNA expression in the ulcer bed by situ hybridization analysis. Conclusion: rhITF can protect gastric mucosa against acute lesion, and enhance the healing of chronic gastric ulcer in the rats.This action may result from the inhibition of gastric acid output, increase of GMBF.Hex and NO content and rhITF stimulated iNOSmRNA expression.
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Objective: To investigate the chemopreventive effects of pioglitazone (exogenous PPAR? ligand) on rat colon aberrant crypt foci, a rat carcinogenesis model induced by dimethylhydrazine (DMH),and to compare pioglitazone with sulindac (a NSAID). Methods: Thirty two, 8 week old, female Sprague Dawley rats were randomly divided into four groups ( n =8 each). Group 1 rats were injected with DMH alone (120 mg?kg -1 , single subcutaneous injection). Group 2 rats were injected with saline alone. Group 3 rats were pre treated with sulindac (320 mg?kg -1 ) for 7 days before DMH initiation. Group 4 rats were treated with pioglitazone (100 mg?kg -1 ). The animals were killed at the end of the experiment (week 5) and the colons were stained with methylene blue. The aberrant crypt foci (ACF) of the colonic mucosa were assessed. Results: In Group 1 rats (DMH only), the average numbers of ACF/colon and AC/colon were (182?93) and (263?198), respectively. In Group 2 (saline group) rats, no ACF were found. In Group 3 (sulindac group) rats, the average numbers of ACF/colon and AC/colon were (91?49) and (140?69), respectively. Both of them were decreased significantly compared with the values in Group 1 ( P
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Objective An investigation was conducted to assess the effects and mechanism of celecoxib [a selective cyclooxygenase(COX) 2 inhibitor] on a rat colitis model induced by trinitrobenzene sulfonic acid (TNBS). Methods The rats were divided into four groups. Group 1 and group 2 were experimental groups. Group 3 and group 4 were control groups. Colitis was induced by intracolonic administration of TNBS (25 mg/ml) in a vehicle of 50% ethanol (0.25 ml) in rats of experiment groups. Three hours before induction of colitis ,the rats were beginning and continuing to treat orally with celecoxib (1.25 mg/kg, group 1) and distilled water (1 ml/0.3 kg, group 2) twice per day for 7 days , respectively. The rats in group 4 were treated orally with celecoxib (1.25 mg/kg) twice per day for 7 days. Group 3 served as healthy control. All rats that survived until the end of the experiment (7 d) were killed and the severity of damage were assessed. The prostaglandin E2 (PGE2) concentrations of colonic mucosa were tested by radioimmunoassay. Results The colonic damage scores were 11.15?3.3 in group 1 and 8.50?2.82 in group 2. Both were significantly higher than that of group 3 (0.62?0.09)( P
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Objective To compare the protective effect of colloidal bismuth subcitrate-1 (CBS-1, Lizudele), or colloidal bismuth subcitrate-2 (CBS-2, De-Nol) and sucralfate against gastric mucosal lesion and to investigate their mechanisms. Methods Gastric mucosal injury of rats was induced by ethanol, stress, aspirin and hydrochloric acid. Gastric ulcer was then induced by 50% acetic acid applied to the gastric tunica serosa. We observed the protective effects against gastric mucosal lesion and measured the injury index and the area of ulcer in each group. Statistical t test was used to compare the difference of each group. Results (1)CBS-1, CBS-2, and sucralfate had protective effect against lesions caused by ethanol, stress, aspirin and hydrochloric acid and could promote acetic acid-induced gastric ulcer healing. (2) The mechanisms of protective effect and ulcer healing promotion were that these drugs could increase gastric blood flow and increase activities of QR, GST and GR, and could also promote overexpression of bFGF mRNA and iNOS mRNA. Conclusion Gastric mucosal protective drugs, CBS and sucralfate had effect of resisting injury and promoting ulcer healing. The mechanisms were that they could increase gastric mucosal blood flow and the expression of bFGF mRNA and iNOS mRNA, and reduce oxygen free radical.
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Objective To investigate the effects of antibody against heat shock protein (HSP) B of Helicobactor pylori (H. pylori) on H.pylori associated gastric disease for the study of the relationship between serum antibody to HSP B of H.pylori and the pathologic changes of the gastric mucosa. Methods 1 036 patients from Shandong province were collected. Six hundred patients were infected with H.pylori. Of those, three hundred received triple therapy for eradication of H.pylori and the other received placebo. Five years later, patients with H.pylori positive chronic superficial gastritis, chronic atrophic gastritis, peptic ulcer, and H.pylori negative chronic superficial gastritis underwent gastroscopy and collected serum specimens again, each group had 20 patients. The Western blot techniques were used to assay antibody to HSP B of H.pylori in sera of these patients. Results The H. pylori positive patients with chronic superficial gastritis ( 0.505 ? 0.061 ) had higher titers of anti H.pylori HSP B IgG antibody compared with those of gastric atrophy ( 0.448 ? 0.105 , P
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0.05) between two groups. Conclusion The results show that the combination of terbinafine and dibazol can improve clinical and mycologic effects and shorten therapeutic course for the treatment of onychomycosis.