首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献,搜索用时 187 毫秒
1.
cAMP在急性胃粘膜损害中的作用的研究   总被引:2,自引:0,他引:2  
本研究应用RIA法,观察了大鼠胃组织的cAMP含量与急性胃粘膜损害之间的关系。结果表明:(1)由消炎痛或失血性休克引起的急性胃粘膜损害时,胃组织cAMP含量明显降低;事先使用异搏定(10mg/kg)可使胃组织cAMP含量明显增加,并使由消炎痛引起的急性胃粘膜损害相应减轻。(2)在正常情况下,胃窦、、胃体组织间cAMP含量并非相等,胃窦部组织cAMP含量高于胃体部组织,与此相应的是急性胃粘膜损害主要  相似文献   

2.
冯康  郭学勤 《生理学报》1997,49(5):491-496
雄性Sprague-Dawley大鼠,用乌拉坦(700mg/kg)和氯醛糖(30mg/kg)腹腔麻醉。在双侧头端延髓腹外侧区(rVLM区)每侧微量注射血管加压素(AVP)(10pmol/0.1μl)可引起平均动脉压(MBP)升高,心率(HR)变化不明显,每侧微量注射AVP的V1受体拮抗剂d(CH2)5[Tyr(Me)^2]AVP(0.1nmol/0.1μl)后MBP和HR无明显变化。若预先在rVL  相似文献   

3.
维拉帕米对大鼠浸水应激性胃溃疡的影响   总被引:6,自引:0,他引:6  
目的和方法:尖激性胃溃疡模型,研究维拉帕米ip对大鼠应激性溃疡的影响及其作用机制。结果:(1)给拉帕米(5~20mg/kg)可抑制大鼠浸水应激性胃溃疡的发生。(2)维拉帕米(10mg/kg)可抑制浸水应激大鼠胃液,胃酸的分泌及胃的运动,而对胃粘液的分泌无影响;(30浸水庆激后大鼠胃粘膜一氧化氮合成酶(NOS)活性和一氧化氮(NO)含量均明显降人氏,维拉帕米(10mg/kg)可抑制应激导致的NOS活  相似文献   

4.
目的:探讨使用外源性肺表面活性物质(PS)治疗能否减轻烟雾吸入所致肺组织细胞损害。方法:Wistar大鼠随机分为5组:Ⅰ组,正常对照;Ⅱ组,烟雾吸入;Ⅲ组,烟雾+PS+机械通气(MV);Ⅳ组,烟雾+盐水+MV;Ⅴ组,烟雾+MV,伤后5min经气管导管注入PS(100mg/kg)或等量盐水,MV4h,观察24h,检测动脉血气、肺水量、支气管肺泡灌洗液(BALF)中白细胞分类计数及乳酸脱氢酶(LDH)、血管紧张素转换酶(ACE)和碱性磷酸酶(AKP)活性、胎盘型碱性磷酸酶(PLAP)含量、肺泡壁纤维成分含量及病理检查等。结果:Ⅱ组伤后发生呼吸衰竭、肺水肿及肺部急性炎症反应,BALF中LDH、AKP、ACE和PLAP水平均明显升高,肺泡壁纤维成分含量显著减少。Ⅲ组血气较Ⅱ组明显改善,但BALF中各酶水平、肺泡壁纤维成分含量及肺部炎症、水肿等无显著减轻。Ⅳ、Ⅴ组治疗无效。结论:烟雾吸入伤早期外源性PS治疗能一定程度改善呼吸功能,但对肺组织细胞损害无明显保护作用,不能减轻继发性炎症反应和急性肺水肿  相似文献   

5.
Vc稀土对肉兔生长性能影响试验研究   总被引:2,自引:0,他引:2  
本文研究Vc稀土对肉兔生长性能的影响。实验结果表明饲料中添加35mg/kg对肉兔有明显增重效果(P〈0.01)。其残留量仅为0.285mg/kg。60mg/kg以下剂量没有引起肉兔体内组织病变。Vc稀土在肉兔体内以骨骼分布为主,其次是分布国胃、肺、脾、肝、肠等组织器官,而在肌肉、心脏组织中含量非常低。  相似文献   

6.
雄性SD大鼠33只,体重180—250g,随机分成四组。正常对照组6只;哌唑嗪组8只,于实验第1、2、3日上午用哌唑嗪灌胃(1mg/kg体重)共3次,第2日下午腹腔注射半乳糖胺(600mg/kg体重)1次,第4日上午处死动物,取肝脏及血清作有关检查;普萘洛尔组及N.S对照组分别用普萘洛尔(2mg/kg体重)及N.S(10ml/kg体重)代替哌唑嗪灌胃,处理程序同哌唑嗪组。结果表明:一、哌唑嗪能显著减轻肝脏病变及血清ALT的升高。二、哌唑嗪对肝损害后肝组织SDH、Mg2+-AT-Pase、ChE、ACP、CCo等酶活性的恢复有显著效果。三、哌唑嗪组LPO明显低于N.S对照组(P<0.01)而SOD活性明显高于N.S对照组(P<0.01)。普萘洛尔组各项指标同对照组比较均无显著差异(P>0.05)。提示:哌唑嗪对大鼠实验性肝损害有一定的保护作用。  相似文献   

7.
反复摄取烟碱对脑肌醇含量的影响   总被引:1,自引:0,他引:1  
急性实验中,间隔5min反复注射烟碱0.5,1.0,1.0,2.0,2.0mg/kgip,30min后大鼠大脑皮层及海马中肌醇含量升高,但纹状体中肌醇含量无显著变化;相同条件下,氯化锂10mmol/kgip30min后大脑皮层和海马中肌醇含量显著降低;慢性实验中,烟碱2.0-10.0mg/kgscbid14d后,大鼠大脑皮层中肌醇含量显著增高;烟碱2.69-11.53mg/kg/dpo64d后,大鼠大脑皮层中肌醇含量也显著增高。表明烟碱的作用不同于氯化锂,反复给予烟碱可使大鼠大脑皮层中肌醇含量增加。  相似文献   

8.
消炎痛可引起小鼠胃粘膜损伤,在一定剂量范围内,其剂量和胃粘膜损伤程度之间有明显的量效关系。在引起胃粘膜损伤时,胃组织胺含量相应增加,大剂量重度损伤时尤为明显。预先用甲氰咪胍灌胃,可明显减轻损伤并降低组织胺含量。提示组织胺参与消炎痛致胃粘膜损伤过程并对损伤产生一定影响。  相似文献   

9.
目的:观察氨茶碱、环磷酸腺苷葡甲胺对兔跨膈压及膈肌电活动的影响,以中肌疲劳的治疗效果提供实难依据。方法:刺激双侧膈神经40min复制膈肌疲劳(DiF)动物模型,动物随机分三组(n=6):氨茶碱组(10mg/kg)、MCA组(10mg/kg),合用组(氨茶碱10mg/kg+葡甲胺cAMP(10mg/kg)。于DiF前、DiF及给药后30、60min记录中压(Pdi);记录膈肌肌电图(EMGdi)并输  相似文献   

10.
全蝎抗癫痫发作敏感性的阿片肽机制   总被引:9,自引:0,他引:9  
红藻氨酸(KainicAcid,KA)癫痫模型,探讨全蝎抗癫痫发作敏感性长期增强的阿片肽机制。本实验选用SD大鼠,随机分为两组,分别给予生理盐水(NS)和全蝎粗提液灌胃10天,10天后两组均分别颈部皮下注射NS和惊厥剂量(10mg/kg)的KA,再分别继续给予NS和全蝎粗提液灌胃10天后,用阈下剂量(5mg/kg)的KA检测癫痫敏感性;用Fos免疫反应活性检测海马结构中神经元的兴奋性;用原位杂交技术检测海马脑啡肽原(PENK)mRNA的动态变化过程。结果显示:实验对照组大鼠癫痫行为敏感性明显增强,脑内癫痫敏感性相关脑区海马齿状回颗粒细胞(DGCs)c-Fos免疫反应阳性细胞数目明显增加,同时海马内具有致癫痫作用的脑啡肽原(PENK)mRNA表达也明显增加;而实验组动物未见上述改变。本工作证实中药全蝎有明显降低海马神经元兴奋性及抗癫痫发作敏感性形成的作用,并提示这很可能与其抑制PENKmRNA表达增加有关  相似文献   

11.
Salicylic acid has been shown to decrease gastric mucosal lesions induced by indomethacin in the rat. In vitro, it has also been shown to counteract the inhibitory effect of indomethacin and aspirin on the cyclooxygenase enzyme system in seminal vesicle microsomes and in platelets and vascular tissue. The hypothesis that the mechanism of salicylic acid "protection" against indomethacin-induced gastric lesions involves interference with indomethacin-induced mucosal cyclooxygenase inhibition was tested. Male, fasted rats were treated with intragastric salicylic acid in doses of 50, 100, 200, 300, or 400 mg/kg concomitantly with a sc injection of 20 mg/kg of indomethacin. Gastric mucosal lesions and mucosal cyclooxygenase activity (as measured by ex vivo prostaglandin F2 alpha synthesis) were examined 3 hr later. Intragastric salicylic acid, 200-400 mg/kg, significantly reduced indomethacin-induced lesion formation, while counteracting significantly indomethacin inhibition of prostaglandin synthesis. Salicylic acid alone did not significantly change cyclooxygenase activity. It is concluded that topical salicylic acid can decrease indomethacin-induced gastric mucosal lesion in the rat, in part, by counteracting the inhibitory effect of indomethacin at the cyclooxygenase level.  相似文献   

12.
Gastric ulcerogenicity and depletion of endogenous prostaglandins (PGs) content induced by tiaprofenic acid, dicrofenac and indomethacin were examined using the same antiinflammatory effective doses. Male Wistar rats were given each of these drugs intragastrically 24, 18, and 3 hrs before sacrifice in the following doses (mg/kg): indomethacin (0.8, 4 and 20); tiaprofenic acid (1.2, 6 and 30); dicrofenac (0.8, 4 and 20). Endogenous prostacyclin (PGI2) and PGE2 in fundic mucosa were determined by radioimmunoassay. The three compounds produced fundic mucosal lesions in a dose-dependent manner. However, tiaprofenic acid and dicrofenac were both less potent than indomethacin in producing gastric mucosal lesions at similar antiinflammatory doses. Mucosal PGE2 content was abolished by the three compounds in the following doses (mg/kg): indomethacin (4 and 20); tiaprofenic acid (6 and 30); dicrofenac (20). Mucosal PGI2 was maintained around 50% of the control value in rats given tiaprofenic acid in a dose of 6 mg/kg or dicrofenac in a dose of 4 mg/kg, while indomethacin in a dose of 4 mg/kg markedly reduced mucosal PGI2 to 17% of the control value. In larger doses, tiaprofenic acid and dicrofenac were also significantly less potent in reducing mucosal PGI2 than indomethacin. These results suggest that the difference in ulcerogenicity between indomethacin and the other two compounds was closely related to their potency in decreasing PGI2 in the gastric (fundic) mucosa.  相似文献   

13.
Gastric ulcerogenicity and depletion of endogenous prostaglandins (PGs) content induced by tiaprofenic acid, dicrofenac and indomethacin were examined using the same antiinflammatory effective doses. Male Wistar rats were given each of these drugs intragasrically 24, 18, and 3 hrs before sacrifice in the following doses (mg/kg): indomethacin (0.8, 4 and 20); tiaprofenic acid (1.2, 6 and 30); dicrofenac (0.8, 4 and 20). Endogenous prostacyclin (PGI2) and PGE2 in fundic mucosa were determined by radioimmunoassay. The three compounds produced fundic mucosal lesions in a dose-dependent manner. However, tiaprofenic acid and dicrofenac were both less potent than indomethacin in producing gastric mucosal lesions at similar antiinflammatory doses. Mucosal PGE2 content was abolished by the three compounds in the following doses (mg/kg): indomethacin (4 and 20); tiaprofenic acid (6 and 30); dicrofenac (20). Mucosal PGI2 was maintained around 50% of the control value in rats given tiaprofenic acid in a dose of 6 mg/kg or dicrofenac in a dose of 4 mg/kg, while indomethacin in a dose of 4 mg/kg markedly reduced mucosal PGI2 to 17% of the control value. In larger doses, tiaprofenic acid and dicrofenac were also significantly less potent in reducing mucosal PGI2 than idomethacin. These results suggest that the difference in ulcerogenicity between idomethacin and the other two compounds was closely related to their potency in decreasing PGI2 in the gastric (fundic) mucosa.  相似文献   

14.
Endothelin-1 (ET-1), nitric oxide, and cytokines are recognized mediators of the inflammatory processes associated with gastric mucosal injury. In this study, we investigated mucosal expression of ET-1, interleukin-4 (IL-4), and the activity of constitutive nitric oxide synthase (cNOS) during indomethacin-induced gastric mucosal injury, and evaluated the effect of antiulcer agents on this process. The experiments were conducted with groups of rats pretreated intragastrically with ranitidine (100 mg/kg), ebrotidine (100 mg/kg), sulglycotide (200 mg/kg) or vehicle, followed 30 min later by an intragastric dose of indomethacin (60 mg/kg). The animals were killed 2 h later and their mucosal tissue subjected to macroscopic damage assessment and the measurements of epithelial cell apoptosis, ET-1, IL-4, and cNOS. In the absence of antiulcer agents, indomethacin caused multiple hemorrhagic lesions and extensive epithelial cell apoptosis, accompanied by a 20.7% reduction in IL-4, a 3.1-fold increase in mucosal expression of ET-1 and a 4.2-fold decline in cNOS. Pretreatment with H2-receptor antagonist, ranitidine produced a 15.7% reduction in the mucosal damage caused by indomethacin, 29.5% decrease in epithelial cell apoptosis and a 19.6% reduction in ET-1, while the expression of IL-4 increased by 10.8% and that of cNOS showed a 2-fold increase. The H2-blocker, ebrotidine, also known for its gastroprotective effects, reduced the indomethacin-induced lesions by 90.2%, epithelial cell apoptosis decreased by 61% and ET-1 showed a 58.2% decline, while IL-4 increased by 30.6% and that of cNOS showed a 3.1-fold increase. Pretreatment with gastroprotective agent, sulglycotide, led to a 51.2% reduction in the extent of mucosal damage caused by indomethacin, a 43.9% decrease in apoptosis, and a 63.5% decrease in ET-1, while the expression of cNOS increased by 3.4-fold and the level of IL-4 showed a 32.2% increase. The results suggest that an increase in vasoconstrictive ET-1 level combined with a decrease in regulatory cytokine, IL-4, and a loss of compensatory action by cNOS may be responsible for gastric mucosal injury caused by indomethacin. Our findings also point to a value of ebrotidine and sulglycotide in countering the untoward gastrointestinal side effects of NSAID therapy.  相似文献   

15.
Rat gastroduodenal mucosa forms prostaglandin (PG) E2. However, little is known about regional differences in PGE2 formation or the effect of gastric hydrochloric acid (HC1) perfusion on regional PGE2 formation. In this study, the rats were divided into 3 groups. Group 1 received intravenous (i.v.), 1 Ml/h, and intragastric (i.g.), 8 ml/h, perfusions of saline simultaneously for 3 h. Group 2 received saline i.v. and 0.15 N HC1 i.g., 8 ml/h. Group 3 was injected with a bolus of asprin (ASA), 60 mg/kg, followed by ASA, 40 mg/kg/h i.v., and 0.15 N HC1 i.g.. The gastric aspirates were analyzed for volume and pH. Segments of gastroduodenal tissue from the fundus, corpus, antrum, and duodenum were minced and then incubated in 1 ml of 5 mM Tris buffer, pH 8.4, for 30 sec with mixing; the incubate was assayed for PGE2 by radioimmunoassay. Intragastric HC1 decreased the pH of aspirate without producing gastric mucosal lesions. However, when combined with i.v. ASA, ulcer formation was present in all animals (p less than 0.05). PGE2 was formed by isolated tissue from four different gastroduodenal regions. The duodenum formed significantly greater amounts than the fundus, antrum, or corpus, which were similar. Intragastric HC1 produced a trend toward increased PGE2 formation (pmol PGE2/mg tissue) in the fundus, 143 +/- 36 to 237 +/- 57; corpus, 87 +/- 13 to 200 +/- 57; antrum, 157 +/- 28 to 224 +/- 65; and duodenum, 235 +/- 56 to 338 +/- 51. However, statistical significance was not reached.  相似文献   

16.
BACKGROUND: Our laboratory group observed earlier that the gastric mucosal cytoprotective effect of prostacyclin (PGI(2)) disappeared after surgical vagotomy in rats. Similarly to this, the beta-carotene induced gastric cytoprotection disappeared in adrenalectomized rats too. AIMS: In these studies we aimed to investigate the possible role of vagal nerve and adrenals in the development of gastric mucosal lesions induced by exogenously administered chemicals (ethanol, HCl, NaOH, NaCl and indomethacin), and on the effects of cytoprotective and antisecretory drugs (atropine, cimetidine), and scavengers (vitamin A and beta-carotene). METHODS: The observations were carried out in fasted CFY strain rats. The gastric mucosal lesions were produced by intragastric (i.g.) administration of narcotising agents (96% ethanol; 0.6 M HCl; 0.2 M NaOH; 25% NaCl) or subcutaneously (s.c.) administered indomethacin (20 mg/kg) in intact, surgically bilaterally vagatomized, and adrenalectomized rats without or with glucocorticoid supplementation (Oradexon, 0.6 mg/kg given i.m. for 1 week). The gastric mucosal protective effect of antisecretory doses of atropine (0.1-0.5-1.0 mg/kg i.g.) and cimetidine (10-25-50 mg/kg i.g.), and vitamin A and beta-carotene (0.01-0.1-1.0-10 mg/kg i.g.) was studied. The number and severity of mucosal gastric lesions was numerically or semiquantitatively measured. In other series of observations the gastric acid secretion and mucosal damage were studied in 24 h pylorus-ligated rats without and with acute bilateral surgical vagotomy. RESULTS: It was found that: (1) the chemical-induced gastric mucosal damage was enhanced in vagotomized and adrenalectomized rats, meanwhile the endogenous secretion of gastric acid, and the development of mucosal damage can be prevented by surgical vagotomy; (2) the gastric cyto- and general protection produced by the drugs and scavengers disappeared in vagotomized and adrenalectomized rats; (3) the gastric mucosal protective effects of drugs and of scavengers returned after sufficient glucocorticoid supplementation of the rats. CONCLUSION: It has been concluded that the intact vagal nerve and adrenals have a key role in the gastric mucosal integrity, and in drugs- and scavengers-induced gastric cyto- and general mucosal protection.  相似文献   

17.
H Matsuda  Y Li  M Yoshikawa 《Life sciences》1999,65(2):PL27-PL32
The roles of capsaicin-sensitive sensory nerves (CPSN), endogenous nitric oxide (NO), sulfhydryls (SHs), prostaglandins (PGs) in the gastroprotection by momordin Ic, an oleanolic acid oligoglycoside isolated from the fruit of Kochia scoparia (L.) SCHRAD., on ethanol-induced gastric mucosal lesions were investigated in rats. Momordin Ic (10 mg/kg, p.o.) potentially inhibited ethanol-induced gastric mucosal lesions. The effect of momordin Ic was markedly attenuated by the pretreatment with capsaicin (125 mg/kg in total, s.c., an ablater of CPSN), N(G)-nitro-L-arginine methyl ester (L-NAME, 70 mg/kg, i.p., an inhibitor of NO synthase), N-ethylmaleimide (NEM, 10 mg/kg, s.c., a blocker of SHs), or indomethacin (10 mg/kg, s.c., an inhibitor of PGs biosynthesis). The attenuation of L-NAME was abolished by L-arginine (300 mg/kg, i.v., a substrate of NO synthase), but not by D-arginine (300 mg/kg, i.v., the enatiomer of L-arginine). The effect of the combination of capsaicin with indomethacin, NEM, or L-NAME was not more potent than that of capsaicin alone. The combination of indomethacin and NEM, indomethacin and L-NAME, or indomethacin and NEM and L-NAME increased the attenuation of each alone. These results suggest that CPSN play an important role in the gastroprotection by momordin Ic on ethanol-induced gastric mucosal lesions, and endogenous PGs, NO, and SHs interactively participate, in rats.  相似文献   

18.
The present paper studies the effect of acetazolamide, an inhibitor of carbonic anhydrase, on acute gastric mucosal damage induced by non-steroidal anti-inflammatory drugs. The study was performed on healthy male subjects. The drugs tested were aspirin (1.5 g/day), indomethacin (75 mg/day), phenylbutazone (600 mg/day) and ibuprofen (600 mg/day) given for 7 days in 3 divided doses. Each drug was given to 5 cases in two separate periods, during which they were given acetazolamide 20 mg/kg/day or placebo in random order. Dyspeptic symptoms were evaluated. Endoscopy was performed before, and 3 and 7 days after NOSAC administration. Gastric mucosal lesions were evaluated according to the scale proposed by Lanza (J. Clin. Pharmacol., 24: 1984, 89) and the severity of the lesions was calculated. All drugs tested produced dyspeptic symptoms and acute mucosal damage of the gastric mucosa. Inhibition of gastric mucosa carbonic anhydrase by acetazolamide cessated promptly dyspeptic symptoms and reduced significantly the number and severity of drug-associated mucosal lesions.  相似文献   

19.
This study was designed to determine the gastroprotective properties of quercetin in ischemia/reperfusion-induced gastric mucosal injury and the involvement of endogenous prostaglandins in this process. Oral pretreatment of rats with quercetin (100 mg x kg(-1)) 30 min before surgery significantly decreased the length of gastric mucosal lesions. However, lower doses of quercetin (25 and 50 mg x kg(-1)) only slightly decreased the gastric mucosal injury. Intraperitoneal application of indomethacin (5 mg x kg(-1)) had no effect in control (sham-operated) animals, but significantly worsened gastric injury in non-treated animals after ischemia/reperfusion. Furthermore, indomethacin only slightly reversed protective effect of quercetin. Non-treated animals showed a marked decrease in adherent mucus after ischemia/reperfusion. On the other hand, application of quercetin prevented this significant decrease even in animals pretreated with indomethacin. It can be concluded that antioxidant properties of quercetin and its mucus protective effect might be the main factors responsible for its protective effect against ischemia/reperfusion-induced gastric mucosal injury.  相似文献   

20.
Rebamipide, a novel antipeptic ulcer drug, 2-(4-chlorobenzoylamino)-3-[2(1H)-quinolinone-4-yl]-propionic acid, was studied for its inhibitory effect on gastric xanthine oxidase activity and type conversion of the enzyme that has a profound role in free radical generation. Intraperitoneal administration of rebamipide at 60 mg/kg body weight reduced gastric mucosal hemorrhagic lesions and lipid peroxidation, which was proportional to the inhibitory effect of rebamipide on alcohol-induced xanthine oxidase-type conversion and enzyme activity. It was also observed that the activity of xanthine oxidase was significantly inhibited by administration of rebamipide at 60 mg/kg body weight, leading to a significant reduction of lipid peroxide content in alcohol-treated rats. The results suggest that alcohol-induced gastric mucosal lesions might be, in part, due to the increased activity of xanthine oxidase and type conversion rate of the enzyme and the protective effect of rebamipide on gastric mucosal lesions would result from its ability to protect against oxidative stress on gastric mucosal lesions of alcohol-treated rats.  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号