川芎嗪对不同状态大鼠胃粘膜血液动力学的影响

用反射光谱法探讨了川芎嗪对不同状态大鼠胃粘膜表层微循环血液量(AEr),Hb氧饱和度(F)的影响,用氢气清除法测定了川芎嗪对胃粘膜微循环障碍大鼠胃粘膜血流量(GMBF)的影响,同时也观察了川芎嗪对出血应激性溃疡形成的作用。结果表明①川芎嗪对正常麻醉大鼠胃粘膜△Er和F值无显著影响,较大剂量时呈一过性下降;②川芎嗪(4mg·100~(-1)g,j.v.)使失血性休克大鼠胃粘膜F值明显增加,注后10分钟时由注前13±10((?)±SD)增至22±5(P<001),△Er不变,表明胃粘膜表层血液灌注明显增加;③川芎嗪能提高LTC_4诱导的胃粘膜微循环障碍时的胃粘膜血流量,注后10分钟时由注前0.521±0.079增至0.979±0.174ml.min~(-1)·100~(-1)g。④川芎嗪对急性失血应激性胃粘膜损伤有保护作用。     

LTC_4(白三烯C_4)对大鼠胃粘膜微循环的影响及其在急性胃粘膜损伤中的作用

近年研究支持LTs是形成消化性溃疡的重要因素之一。本文用Wistar系雄性大鼠为研究对象,将LTC_4溶液(日本)用氮气饱和生理盐水稀释,按0.1ng·100g~(-1)剂量经尾静脉注射。观察项目和结果如下:1.用实体显微镜(Nikon UFX-Ⅱ)活体观察胃粘膜表层微血管图象。注后迅速出现严重微循环变化,粘膜苍白,毛细血管和     

酒精致大鼠胃粘膜微循环变化及早期血管损伤的研究

本文研究了酒精所致大鼠胃粘膜微循环变化及早期血管的损伤。结果表明：60％酒精灌胃后可致胃粘膜血液灌注量及血流量明显增加，血红蛋白氧饱和度显著下降。60％和100％酒精灌胃后3分钟内即引起胃粘膜血管损伤（单星蓝染色标记）和通透性增强。100％酒精灌胃后1分与30分相比血管损伤面积基本未变，但组织出血性坏死区面积明显增加且接近血管损伤面积。结果提示：胃粘膜血管的损伤是酒精致胃出血性坏死形成的早期病因之一。     

拟肾上腺素能及抗肾上腺素能药对胃粘膜微循环的作用

本文观察了拟肾上腺素能及抗肾上腺素能药物对小鼠胃粘膜微循环的影响,结果表明,①去甲肾上腺素可引起胃粘膜细静脉、毛细血管明显收缩;毛细血管数减少;血流明显减慢,甚至血流停滞;红细胞明显聚集。②大剂量多巴胺可兴奋胃粘膜微血管α-受体,使细静脉、毛细血管收缩,血流减慢,但其作用持续较短。③     

乙醇性胃粘膜损伤大鼠胃粘膜血液动力学变化及丹参提取物-F的作用

目的 :探讨不同浓度乙醇以及在事先给予丹参提取物 F ( DSE-F)和消炎痛的情况下大鼠胃粘膜血液动力学变化。方法 :用组织反射光谱分析仪 ( TS-2 0 0 )测定胃粘膜表层血液量 ( ΔEr)和 Hb氧饱和度 ( F)。结果 :( 1)胃粘膜损伤程度随乙醇浓度增高而加大 ;( 2 )低浓度乙醇引起胃粘膜充血 ,而高浓度则导致静脉淤血 ;( 3 )乙醇诱导的胃粘膜血液动力学变化因预先给予 DSE-F或消炎痛而减轻。结论 :( 1)乙醇性胃粘膜损伤的致病因素是高浓度乙醇所致的胃粘膜淤血缺氧 ;( 2 ) DSE-F对乙醇性胃粘膜损伤的保护作用在于减轻乙醇所致的胃粘膜血液动力学变化 ,后者可能与内源性前列腺素有关。     

蝎毒活性多肽对大鼠肠系膜微循环的影响

目的 :研究蝎毒活性多肽对大鼠肠系膜微循环的影响。方法 :Dextran(分子量 480 0 0 0 ) 60 0mg/kg静脉注射制备大鼠肠系膜急性微循环障碍 (AMD)模型 ,采用活体微循环法观察肠系膜微循环细动、静脉血流速度 (ABFV ,VBFV)、血流状态 (BFS)、血管口径 (AD、VD)的变化。结果 :SVAPs 0 .0 7mg/kg、Nif 0 .0 5mg/kg静注可使ABFV增大各为 1 1 %、1 2 .3% ,VBFV则为 1 2 .5 %、1 2 .6% ,BFS改善 ,AD增加 2 0 %、36.8% ,VD增加 1 1 .7%、2 8% ,CN增多 ,静注SVAPs可明显逆转AMD。结论 :SVAPs可明显改善肠系膜微循环 ,并对Dextran诱导的AMD具有拮抗作用。     

用激光多普勒血流仪检测门静脉高压兔的胃粘膜血流量

目的研究门静脉高压症胃粘膜微循环血流量的变化。方法22只兔随机分成2组:门静脉高压模型组(PHT组)11只,通过门静脉部分结扎产生门静脉高压症;假手术组(SO组)11只,仅分离门静脉主干而不结扎。4周后用激光多普勒血流仪(Laser Doppler Flowmetry,LDF)检测胃底、胃窦的粘膜血流量,比较两组间的差异。结果 PHT组胃底、胃窦的粘膜血流量分别为(73.44±25.47)BPU.(97.85±15.05)BPU;SO组相应部位的粘膜血流最为(136.38±18.40)BPU,(89.85±20.34)BPU。PHT组胃底粘膜血流量明显低于SO组(P<0.01),而其胃窦的粘膜血流量与SO组相比稍低,但不具有统计学意义(P>0.05)。结论门脉高压时胃粘膜的血流量降低.     

植物油对大鼠应激性胃粘膜损伤的保护作用

如所周知,摄入脂肪能抑制胃酸分泌,但脂肪对应激性胃粘膜损伤是否有保护作用尚未见报道。本工作将大鼠捆缚后置于4℃冻箱3小时造成应激性胃粘膜损伤,观察到植物油有保护胃粘膜免于损伤的作用:(1)     

环氧合酶-2抑制剂对盐酸诱导大鼠胃粘膜损伤后上皮细胞增殖和愈合的影响

目的:探讨特异性和非特异性环氧合酶-2(COX-2)抑制剂,对盐酸诱导胃粘膜损伤后上皮细胞增殖和损伤愈合的影响。方法:大鼠胃内给予06mol/LHCl1mL后,胃内给予NS-398或吲哚美辛,Westernblot和免疫组化法分析盐酸灌胃前、后胃粘膜COX-2表达,免疫组化检测增殖细胞核抗原(PCNA)评价上皮细胞的增殖状态,小格图纸法计算胃损伤指数(LI)。结果:盐酸灌胃后,COX-2在胃粘膜表层上皮细胞和腺颈部成体干细胞高表达。盐酸灌胃后24h,NS-39840mg/kg组及吲哚美辛组PCNA标记指数(PCNA-LI)分别为(22.72±4.33)%和(21.98±5.18)%,明显低于对照组(34.46±3.61)%(P<0.05);NS-3984mg/kg组和40mg/kg组LI分别为(1.28±0.58)%和(1.16±0.56)%,显著高于对照组(0.58±0.24)%(P<0.05)。结论:COX-2抑制剂抑制胃粘膜上皮细胞增殖,延迟大鼠胃粘膜损伤的愈合,提示COX-2表达在胃粘膜再生过程中起重要作用。     

小鼠树突细胞LTB4-BLT的表达

目的探讨树突细胞(DC)白三烯B4(LTB4)-白三烯B4受体(BLT)信号通路LTB4-BLT(包括LTB4-BLT1和LTB4-BLT2)存在状态。方法分离正常小鼠骨髓细胞,体外用细胞因子(IL-4,GS-CSF)诱导、分化为DC,脂多糖(LPS)刺激其成熟。光镜观察细胞形态和流式细胞术进行DC表型分子鉴定。ELISA方法检测幼稚、成熟DC培养液中LTB4含量;RT-PCR方法检测幼稚和成熟DC BLT1和BLT2 mRNA表达。结果DC培养的2、4和6 d(DC幼稚状态)及8 d(LPS刺激后DC成熟状态),培养液中LTB4含量分别为(10.667±2.394)ng/L、(7.089±1.810)ng/L、(3.222±0.995)ng/L及(14.217±3.396)ng/L。随DC分化进程,培养液中LTB4含量呈递减趋势,而成熟DC分泌LTB4含量比幼稚DC明显增高(P<0.05);RT-PCR示成熟状态和幼稚状态DC均表达BLT1和BLT2 mRNA,且成熟比幼稚状态DC mRNA表达水平增强(P<0.05)。结论DC可通过分泌LTB4和表达BLT而建立自身LTB4-BLT信号通路,为进一步研究DC LTB4-BLT1和LTB4-BLT2这2条信号通路在炎症反应和免疫调节中的作用提供了实验依据。     

Observer agreement on the grading of gastric atrophy

AIMS: Assessment of lesser or doubtful degrees of gastric atrophy can be difficult, especially in the antrum, since well established criteria are lacking. At the Houston Working Party on Gastritis in 1994 a visual analogue scale was designed for the grading of histopathological parameters. This was done to promote uniformity in grading by acting as a reference. The purpose of the present study was to measure interobserver variation between pathologists familiar with the Houston visual analogue scale in a specifically selected set of biopsies from patients with lesser or doubtful degrees of atrophy. METHODS AND RESULTS: Thirty cases with biopsies of the antrum and corpus from a long-term follow-up study on Helicobacter pylori gastritis comprised the current study material. The cases were selected from that study because there had been uncertainty or disagreement on the presence of gastric atrophy. The study set of haematoxylin and eosin (H & E) slides was circulated amongst gastrointestinal pathologists familiar with the visual analogue scale who were unaware of the source of the study set nor had any other clinical information. Interobserver variability was analysed using kappa statistics. The overall agreement for the grade of atrophy in antral biopsies was 0.461; the kappa value was 0.18 (95% confidence limits 0.12-0.24), which is considered poor agreement. The kappa value was nevertheless statistically significant (P < 0. 01). The overall agreement on the grade of atrophy in the corpus biopsies was apparently good (0.833), but the kappa which adjusts for chance agreement was only moderate (0.48; 95% confidence limits 0.42-0.55; P < 0.001). CONCLUSION: The studied series comprised a self-selected sample in which there was doubt about the grade of atrophy and such a sample will produce lower kappa values than a random sample of gastric biopsies. The results nevertheless confirm that better guidelines and firm criteria are needed to properly diagnose and grade gastric atrophy. It is suggested that the use of two grades, low- and high-grade atrophy, akin to that in use for grading inflammatory bowel disorder (IBD)- associated dysplasia, could improve agreement. Furthermore optimal biopsy quality with full thickness mucosa and proper orientation appears important for grading gastric atrophy.     

胃上皮异型增生及胃癌组织中细胞凋亡的原位观察

目的　探讨胃癌前病变和胃癌组织中细胞凋亡的情况。方法　采用TUNEL技术检测胃上皮异型增生及胃癌组织中的细胞凋亡率。结果　在不能肯定为异型增生中凋亡率为 2 1 94%± 5 4 8%;低度异型增生的凋亡率为 2 3 70 %± 4 13%;高度异型增生中凋亡率为 18 0 5 %± 3 99%,随着胃黏膜细胞异型程度的增高 ,细胞凋亡反而逐渐减少 ,而在浸润癌其凋亡率进一步减少为 8 13%± 1 98%。结论　在胃黏膜从异型增生到癌变过程中可能存在细胞凋亡的被抑制 ,应该凋亡的异常细胞得以长期生存 ,这些细胞对致突、致癌剂的易感性升高 ,基因更易发生突变 ,增加了胃黏膜细胞恶变的机会。     

胃体和胃窦部体表胃电电极定位观测

本文采用 X 线胃肠钡餐摄片法,以胃体及胃窦部中央为胃体点和胃窦点.100名正常人测量结果:胃体点在剑突至脐连线中点上方平均1.6cm,旁开左侧4.5cm 处;胃窦点在剑突至脐连线中点下方0.7cm,旁开右侧1.4cm 处。     

Gastroscopic treatment of gastric band penetrating the gastric wall

Gastric wall penetration of a gastric band after operation for morbid obesity is a well known late complication. The treatment is usually reoperation. In this case report we show that a band penetrating the gastric wall can be successfully treated by gastroscopic operation. This technique is more simple than reoperation, especially in case of morbid obesity at the time of the complication.     

Effects of caerulein on the gastric motility of rats

The effects of caerulein on gastric motility in urethane-anesthetized rats were studied. Caerulein administered into the lateral cerebral ventricle (i.c.v.) and jugular vein (i.v.) caused predominantly an inhibitory effect on gastric motility but sometimes an excitatory or a biphasic effect. The inhibitory response was reduced after vagotomy and/or splanchnicotomy, or after guanethidine. The remaining inhibitory response was abolished by tetrodotoxin, but was resistant to atropine and guanethidine. The excitatory response was abolished by atropine. Discharges of the gastric branch of the vagus nerve were decreased by i.v. injection of caerulein but increased by i.c.v. injection, whereas those of the splanchnic nerve were increased by both i.v. and i.c.v. injection. These results suggest that caerulein causes an inhibition of gastric motility by centrally stimulating vagal non-adrenergic inhibitory nerves and splanchnic adrenergic nerves and inhibiting vagal cholinergic nerves, and by peripherally stimulating non-adrenergic inhibitory neurons of the myenteric plexus. This peptide causes an excitation by stimulating cholinergic neurons of the myenteric plexus.