高频电磁场曝露对胃粘膜急性损伤的 治疗效应及作用机制研究

目的：探讨高频电磁场曝露对大鼠胃粘膜急性损伤的治疗效应,以及血管内皮素1（endothelin-1,ET-1）、一氧化氮（nitric oxide,NO）及超氧化物岐化酶（superoxide dismutase,SOD）在高频电磁场这一效应中的作用。方法：SD大鼠胃粘膜急性损伤模型采用indomethaein灌胃法复制,高频电磁场曝露的条件为频率40．68MHz,电流输出30—50mA,曝露15min,1／d,对照组电磁场曝露条件相同,但无电流输出,观察电磁场曝露1或6次后大鼠胃粘膜损伤程度以及血浆ET-1、NO和SOD水平的变化。结果：电磁场曝露1次后,急性胃损伤大鼠胃粘膜损伤程度较对照组并无显著性差异（p〉0．05）,血ET-1和NO水平均明显增高（P均〈0．05）;曝露6次后,胃粘膜损伤程度较对照组明显改善（P〈0．05）,但血ET-1和NO水平则与对照组无显著性差异（P〉0．05）,血SOD水平在电磁场曝露1或6次后均无显著意义的变化（P均〉0．05）。结论：40．68MHz高频电磁场30—50mA曝露对大鼠胃粘膜急性损伤,呈现出有效的治疗效应,高频电磁场这一作用机制与ET-1、NO及SOD无关。     

腹部恒磁场作用对大鼠药物性胃损伤的治疗机制探讨

目的：观察腹部恒磁场治疗急性药物性胃损伤模型的同时,大鼠胃粘膜组织内皮素1（endothelin—1,ET-1）、一氧化氮（nitric oxide,NO）、谷胱甘肽过氧化物酶（glutathione peroxidase,GSH—Px）及超氧化物岐化酶（superoxide dismutase,SOD）的水平,探讨磁场治疗胃损伤的作用机制。方法：10只健康SD大鼠,在Indomethacin胃灌注法复制急性胃损伤模型后,以钡铁氧体恒磁场（表面磁强度为1300—1600GS）作用大鼠腹部3小时,观察胃损伤指数及病理损伤积分,同时对胃粘膜组织中ET-1、NO、GSH—Px及SOD水平进行比较。结果：腹部磁场作用3小时后,大鼠胃损伤指数及病理损伤积分均显著减轻（P均〈0．05）;胃粘膜组织内ET-1、NO及GSH—Px水平均无显著改变（p均〉0．05）,SOD含量较对照组均明显升高（P〈0．05）。结论：恒磁场（1300—1600CS）腹部作用3小时,大鼠急性胃损伤程度可明显减轻,磁场对胃粘膜组织内自由基的影响可能参与其作用机制。     

磁场对急性胃损伤的治疗效应及其机制的实验研究

目的：探讨腹部恒磁场作用,对大鼠急性胃损伤模型的治疗效应及其作用机制.方法：10只健康SD大鼠,以indomethacin胃灌注法复制急性胃损伤模型,以表面磁强度为1300-1600GS,钡铁氧体恒磁场作用大鼠腹部3小时,观察胃损伤指数及病理损伤积分,同时对血浆中内皮素（endothelin,ET）、一氧化氮（nitric oxide,NO）、谷胱甘肽过氧化物酶（GSH-Px）及超氧化物岐化酶（SOD）水平进行比较.结果：恒磁场腹部作用后,大鼠胃损伤指数及病理损伤积分较对照组均显著减轻（p均〈0.05）;血浆ET-1和NO水平却无无明显改变（p均〉0.05）,血GSH-Px和SOD含量较对照组均明显升高（p均〈0.05）.结论：腹部1300-1600GS恒磁场作用3小时,对大鼠急性胃损伤具有明显的治疗效应,磁场的这一效应可能与其增加血浆中清除氧自由基的GSH-Px和SOD活性有关.     

一氧化氮/内皮素在大鼠胃粘膜损伤中的作用及电针的调整效应

用酒精灌胃引起大鼠胃粘膜损伤模型,观察内皮衍生因子（ＮＯ／ＥＴ）的含量变化和电针对胃粘膜损伤调整作用,结果发现：酒精灌胃后,胃粘膜血流量（ＧＭＢＦ）、跨壁电位差,血ＮＯ含量降低（Ｐ〈０．０１）,血浆ＥＴ含量和胃粘膜损伤指数（ＬＩ）增高（Ｐ〈０．０１）。Ｌ－精氨酸（Ｌ－Ａｒｇ）或硝普钠（ＳＮＰ）灌注预处理后（ｉｖ）,ＮＯ含量和ＧＭＢＦ明显升高（Ｐ〈０．０１）,ＥＴ含量和ＬＩ指数下降（Ｐ〈０．０１）。     

肾血管性高血压大鼠模型中ET1和CGRP的变化

目的探讨降钙素基因相关肽（CGRP）及血浆内皮素（ET1）在高血压病中的作用。方法选用正常血压大鼠42只,随机分对照组、手术组、假手术组,分别观察血压值、CGRP及ET1值。结果手术组与正常组比较血压明显高于正常对照组（P〈0．01）,假手术组与正常对照组比较,血压无明显变化（P〉0．05）;手术组与对照组比较CGRP显著升高（P〈0．01）;假手术组与正常对照组比较,CGRP未见升高（P〉0．05）。手术组与对照组比较ET1无明显变化（P〉0．05）。结论CGRP在肾血管性高血压的发生发展中具有保护作用。ET1与CGRP是心血管系统中的一对拮抗因子,与CGRP的作用相反,ET1有较强的缩血管作用,从而导致血压升高。     

慢性温和应激抑郁模型大鼠5-羟色胺、色氨酸和应激激素的变化

目的：通过观察慢性温和应激对大鼠行为及5-羟色胺、色氨酸、应激激素的影响,进一步阐明应激致抑郁发生的机制。方法：利用慢性不可预计温和应激（CUMS）结合行为学指标建立大鼠抑郁动物模型;高效液相检测血浆和脑5-HT、儿荼酚胺;放免方法检测血浆皮质醇换算成皮质酮含量;氨基酸分析仪检测血清色氨酸的含量。结果：①CUMS诱导8周大鼠糖水偏爱性与对照组相比明显减低（P〈0．05）;体重和旷场实验评分下降（P〈0．05）。②CUMS诱导8周大鼠大脑和血浆5-HT含量显著下降（P〈0．05）;而血清色氨酸含量与对照组相比则明显升高（P〈0．05）。③CUMS诱导8周大鼠血浆去甲肾上腺素和肾上腺素含量与对照组相比明显升高（P〈0．05）：血浆皮质酮含量与对照组相比统计学上无显著性差异（P〉0．05）。结论：利用CUMS建立的抑郁模型大鼠存在着神经内分泌紊乱,CUMS大鼠抑郁样行为的发生可能与血浆去甲肾上腺素和肾上腺素升高对色氨酸代谢的影响有关。     

致炎剂联合降钙素基因相关肽对大鼠硬脑膜神经源性炎症的影响

目的：探讨致炎剂联合降钙素基因相关肽对大鼠硬脑膜神经源性炎症的影响,寻求最佳慢性偏头痛的实验模型。方法：24只SD雄性大鼠。随机分为生理盐水组（NS）、降钙素基因相关肽组1（CGRe1,10-3M）、降钙素基因相关肽组2（CGRP2,10-4M）,以及IS（20μL）＋CGRP（10μL,10-4M）组,每组各6只,通过甲苯胺蓝染色法,观察肥大细胞脱颗粒,采用伊文氏蓝荧光显像法,观察大鼠硬脑膜血管渗出,采用多普勒激光血流仪检测法,观察各组硬脑膜动脉血流量变化。结果：与NS组相比,CGRPl、CGRP2、IS＋CGRP组肥大细胞脱颗粒数和比率、脑血流量均明显升高,P〈0．05,并且硬脑膜荧光红斑明显增多;与CGRPl、CGRP2组相比,IS＋CGRP组肥大细胞脱颗粒数和比率、脑血流量均明显升高,P〈0．05,并且硬脑膜荧光红斑明显增多。CGRP两组相比,上述指标比较,差异没有统计学意义,P〉0．05。结论：IS＋CGRP能够明显刺激大鼠硬脑膜发生神经源性炎症反应,可以作为慢性偏头痛动物实验模型。     

即刻电针介入对IBS模型大鼠血浆ET,CGRP水平及结肠ETR-A,CGRPmRNA表达的影响

目的：比较即刻电针天枢穴、足三里穴对肠易激综合征（ms）模型大鼠血浆降钙基因相关肽（CGRP）、内皮素（ET）水平及结肠组织中内皮素受体A（ETR－A）、CGRPmRNA表达的影响,旨在探讨电针即刻治疗IBS的部分机制。方法：采用WISTAR幼鼠制备肠易激综合征模型,随机分为空白对照组、模型组、天枢组、足三里组,每组8只。空白对照组不作任何处理,模型组只束缚不针刺,天枢组和足三里组在实验第8周电针治疗一次,留针20min。治疗结束后处死大鼠,取大鼠血浆及部分结肠组织进行生物活性物质检测。采用酶联免疫法检测血浆中CGRP、ET、结肠组织中ETR—A的含量,采用RT—PCR法检测结肠组织中CGRPmRNA表达。结果：（1）即刻电针对IBS模型大鼠血浆CGRP、ET水平的影响：与空白对照组比较,模型组CGRP水平明显降低（P〈0．01）;与模型组比较,天枢组、足三里组CGRP水平明显升高（P〈0．01）。与空白对照组比较,模型组ET水平升高（P〈0．05）;与模型组比较,天枢组ET水平明显降低（P〈0．01）。（2）即刻电针对IBS模型大鼠结肠组织ETR—A水平的影响：与空白对照组比较,模型组ETR—A水平明显升高（P〈0．01）;与模型组比较,足三里组ETR-A水平明显降低（P〈0．01）。（3）即刻电针对IBS模型大鼠结肠组织CGRPmRNA表达的影响：与空白对照组比较,模型组、天枢组、足三里组CGRPmRNA表达明显增强（P〈0．01,P〈0．05）;与模型组比较,足三里组CGRPmRNA表达减弱（P〈0．05）。结论：即刻电针介入后,能够调节机体的内环境紊乱和CGRP、ET的平衡失调。这种调节作用因穴位不同而具有不同的特点,天枢穴对血浆中CGRP、ET调节作用较强,足三里穴在受体和基因表达方面作用明显。     

胰岛素对阿尔茨海然病大鼠血浆血小板活化因子及海马突触可塑性的影响

目的：探讨胰岛素对阿尔茨海默病（AD）大鼠血浆血小板活化因子（PAF）及海马突触可塑性的影响。方法：将30只SD大鼠随机分为治疗组（10只）、模型组（10只）、假手术组（10只）,采用侧脑室注射链脲霉素（STZ）建立AD大鼠模型。治疗组大鼠皮下注射胰岛素（0．1U／kg）,模型组及假手术组大鼠皮下注射等体积的生理盐水（1mL／kg）。通过Morris’s水迷宫实验评估各组大鼠的认知功能,酶联免疫吸附法测定各组大鼠的血浆PAF含量,免疫印迹法检测大鼠海马突触素的表达。结果：治疗4周后,模型组大鼠连续4天水迷宫的潜伏期均显著长于假手术组大鼠（P〈0．05）,而治疗组大鼠第2、3、4天水迷宫潜伏期均较模型组显著缩短（P〈0．05）,但仍长于假手术组大鼠（P〈0．05）;模型组大鼠的血浆PAF含量和海马突触素的表达均显著高于假手术组,而治疗组大鼠的血浆PAF含量和海马突触素的表达均显著低于模型组（P〈0．05）,差异均有统计学意义（P〈0．05）。结论：皮下注射胰岛素可改善AD大鼠的认知功能,这可能与其下调AD大鼠血浆PAF水平以及保护突触的可塑性有关。     

亚低温治疗急性重度颅脑损伤120例临床疗效分析

摘要目的：研究亚低温治疗对于急性重度颅脑损伤临床疗效。方法：将226例急性重度颅脑损伤患者随机分为治疗组与对照组。治疗组120例,对照组106例。对照组采用颅脑损伤常规治疗。治疗组在对照组基础上加用亚低温治疗。观察两组患者治疗前后颅内压、血糖变化。对比两组患者治疗前后GCS评分、GOS评分及不良反应发生率。结果：治疗组于治疗1d、3d及7d时颅内压与血糖值均明显低于对照组（P〈0．01）。治疗3个月时治疗组平均GCS评分明显高于对照组（P〈0．01）;治疗组恢复良好比例高于对照组（P〈O．05）,而死亡率低于对照组（P〈0．05）。两组患者治疗不良反应发生率无明显区别（P〉0．05）。结论：采用亚低温疗法有助于辅助降低急性重度颅脑损伤患者颅内压及血糖,保护脑细胞,改善患者预后,降低死亡率。     

Effect of peripherally-injected glucagon-like peptide-1 on gastric mucosal blood flow

The aim of this study was to investigate the mechanisms involved in the effect of glucagon-like peptide-1 (GLP-1) on the decrease in gastric mucosal blood flow (GMBF) induced by intragastric ethanol.After preparation of the stomach for GMBF recording, a probe was placed to the gastric mucosa and basal GMBF recordings were obtained by a laser Doppler flowmeter after a 30-minute stabilization period. Following GLP-1 (1000 ng/kg; i.p.) injection, 1 ml of absolute ethanol was applied to the gastric chamber and GMBF was recorded continuously during a 30-minute period. GLP-1 (1000 ng/kg; i.p.) prevented the decrease in GMBF induced by ethanol. Nitric oxide (NO) synthase inhibitor L-NAME, (30 mg/kg; s.c.), calcitonine gene-related peptide (CGRP) receptor antagonist CGRP-(8–37) (10μg/kg; i.p.), and cyclooxygenase inhibitor indomethacin (5 mg/kg; i.p.) all inhibited the GMBF-improving effect of GLP-1.We concluded that, NO, CGRP and prostaglandins may be involved in the effect of peripherally-injected GLP-1 on GMBF reduction induced by intraluminal ethanol.     

失血性休克大鼠模型的改进及胃黏膜血流量的测定

目的探讨失血性休克大鼠模型的建立及胃黏膜血流量的测定。方法16只健康雄性SD大鼠随机分为两组：对照组（n=8）、失血性休克组（n=8）。失血性休克组使用颈动脉失血-颈静脉失血回输的方式制备失血性休克大鼠模型。维持平均动脉压40mmHg 1h后复苏,复苏后2h动物模型制作成功。使用激光多普勒血流仪测定大鼠胃黏膜血流量;采用光镜及透射电镜观察胃黏膜损伤情况。结果失血性休克组胃黏膜血流量较对照组明显降低,差异非常显著（P〈0．01）,胃黏膜细胞坏死、脱落、溶解,局部溃疡形成。结论失血性休克大鼠胃黏膜血流量明显降低,存在广泛的胃黏膜损伤。     

Gastroprotective and vasodilatory effects of epidermal growth factor: the role of sensory afferent neurons

Epidermal growth factor (EGF) has been shown to exert gastric hyperemic and gastroprotective effects via capsaicin-sensitive afferent neurons, including the release of calcitonin gene-related peptide (CGRP). We examined the protective and vasodilatory effects of EGF on the gastric mucosa and its interaction with sensory nerves, CGRP, and nitric oxide (NO) in anesthetized rats. Intragastric EGF (10 or 30 microg) significantly reduced gastric mucosal lesions induced by intragastric 60% ethanol (50.6% by 10 microg EGF and 70.0% by 30 microg EGF). The protective effect of EGF was significantly inhibited by pretreatment with capsaicin desensitization, human CGRP1 antagonist hCGRP-(8-37), or N(omega)-nitro-L-arginine methyl ester (L-NAME). Intravital microscopy showed that topically applied EGF (10-1,000 microg/ml) dilated the gastric mucosal arterioles dose dependently and that this vasodilatory effect was significantly inhibited by equivalent pretreatments. These findings suggest that EGF plays a protective role against ethanol-induced gastric mucosal injury, possibly by dilating the gastric mucosal arterioles via capsaicin-sensitive afferent neurons involving CGRP and NO mechanisms.     

小柴胡汤加减联合奥美拉唑对慢性胃炎具有治疗增效作用

本研究选取本院收治的慢性胃炎患者114例并根据治疗方法不同分为对照组和观察组。对照组患者采用奥美拉唑治疗,观察组患者采用奥美拉唑联合小柴胡汤加减治疗,分析小柴胡汤加减联合奥美拉唑对慢性胃炎血清表皮生长因子(EGF)、胃黏膜氧化酶-2 (COX-2)蛋白表达情况的影响及护理对策。研究结果表明,治疗前两组患者胃镜检查充血水肿、糜烂、黏膜白相、颗粒增生发生率比较无统计学差异(p>0.05);治疗后,观察组患者各项指标发生率低于对照组(p<0.05);治疗前,两组患者血清EGF、Bcl-2、CRP和胃黏膜COX-2、P-p65表达水平比较无统计学差异(p>0.05),治疗后发现观察组患者血清EGF水平高于对照组,血清Bcl-2、CRP和胃黏膜COX-2、P-p65表达水平低于对照组(p<0.05);治疗前,两组患者在躯体功能、躯体职能、躯体疼痛、情感职能、心理健康评分等生活质量评分上比较无统计学差异(p<0.05),治疗后,观察组患者各项评分高于对照组(p>0.05)。本研究初步结论说明,小柴胡汤加减联合奥美拉唑治疗慢性胃炎疗效显著,可改善患者血清EGF、Bcl-2和胃黏膜COX-2表达水平,提高患者生活质量。     

Gastroprotective action of orexin-A against stress-induced gastric damage is mediated by endogenous prostaglandins, sensory afferent neuropeptides and nitric oxide

Orexin-A, identified in the neurons and endocrine cells in the gut, has been implicated in control of food intake and sleep behavior but little is known about its influence on gastric secretion and mucosal integrity. The effects of orexin-A on gastric secretion and gastric lesions induced in rats by 3.5 h of water immersion and restraint stress (WRS) or 75% ethanol were determined. Orexin-A (5-80 microg/kg i.p.) increased gastric acid secretion and attenuated gastric lesions induced by WRS and this was accompanied by the significant rise in plasma orexin-A, CGRP and gastrin levels, the gastric mucosal blood flow (GBF), luminal NO concentration and an increase in mRNA for CGRP and overexpression of COX-2 protein and the generation of PGE(2) in the gastric mucosa. Orexin-A-induced protection was abolished by selective OX-1 receptor antagonist, vagotomy and attenuated by suppression of COX-1 and COX-2, deactivation of afferent nerves with neurotoxic dose of capsaicin, pretreatment with CCK(2)/gastrin antagonist, CGRP(8-37) or capsazepine and by inhibition of NOS with L-NNA. This study shows for the first time that orexin-A exerts a potent protective action on the stomach of rats exposed to non-topical ulcerogens such as WRS or topical noxious agents such as ethanol and these effects depend upon hyperemia mediated by COX-PG and NOS-NO systems, activation of vagal nerves and sensory neuropeptides such as CGRP released from sensory nerves probably triggered by an increase in gastric acid secretion induced by this peptide.     

Mast cell stabilizator and antioxidant effects of epidermal growth factor (EGF) on gastric mucosal injury induced by ethanol in rats

The role of epidermal growth factor (EGF), a polypeptide containing 53 amino acids, on protection and repair of ethanol-induced gastric mucosal injury was investigated in rats. In addition, the effects of EGF on the gastric damage were evaluated histopathologically. We used 48 Spraque-Dawley rats which were divided into [corrected] three groups as control rats, ethanol treated rats and ethanol+EGF treated rats. The ethanol group was given a gastric gavage containing 1 ml of 80% ethanol (v/v) prepared in distilled water. EGF (100 microg/kg) was given by intragastric gavage 30 min before the administration of ethanol. We studied histopathological evaluation and the histochemical heterogeneity of mast cells and its degree of degranulation. Besides, gastric tissue malondialdehyde (MDA), protein sulfhydryl groups (SH), and protein carbonyl levels were measured. EGF treatment stabilized mast cells degranulation and had lower polymorphonuclear leukocytes (PMNL) infiltration, ulcer index, histamine, and MDA; protein carbonyl levels were also lower, compared to the non-treated animals. EGF exerts a protective effect on gastric mucosa to ethanol-induced gastric injury probably through antioxidant and mast cell stabilizing mechanism.     

Exogenous and endogenous ghrelin in gastroprotection against stress-induced gastric damage

Ghrelin, identified in the gastric mucosa has been involved in control of food intake and growth hormone (GH) release but little is known about its influence on gastric secretion and mucosal integrity. The effects of ghrelin on gastric secretion, plasma gastrin and gastric lesions induced in rats by 75% ethanol or 3.5 h of water immersion and restraint stress (WRS) were determined. Exogenous ghrelin (5, 10, 20, 40 and 80 microg/kg i.p.) increased gastric acid secretion and attenuated gastric lesions induced by ethanol and WRS and this was accompanied by the significant rise in plasma ghrelin level, gastric mucosal blood flow (GBF) and luminal NO concentrations. Ghrelin-induced protection was abolished by vagotomy and attenuated by suppression of COX, deactivation of afferent nerves with neurotoxic dose of capsaicin or CGRP(8-37) and by inhibition of NOS with L-NNA but not influenced by medullectomy and administration of 6-hydroxydopamine. We conclude that ghrelin exerts a potent protective action on the stomach of rats exposed to ethanol and WRS, and these effects depend upon vagal activity, sensory nerves and hyperemia mediated by NOS-NO and COX-PG systems.