血管内皮生长因子在门脉高压患者胃黏膜的表达

目的探讨血管内皮生长因子(VEGF)在肝硬化门脉高压(PHT)患者胃黏膜的表达及其在门脉高压性胃病(PHG)发病中的作用。方法分别采集PHG、PHT和正常对照组胃黏膜组织。应用免疫组化法检测胃黏膜VEGF蛋白的表达。PHG程度按改良的McMrmark’s分级由有经验的消化科医师盲法评估。结果PHG组(49.56%±12.26%)和PHT组(48.56%±12.23%)胃黏膜VEGF表达较正常对照组(5.11%±2.14%)显著性增高(P<0.05),但前两组间VEGF的表达无统计学差异(P>0.05)。VEGF阳性表达主要见于胃小凹颈部黏膜细胞浆内。VEGF与PHG积分呈显著性正相关(H=10.592,P<0.05)。结论肝硬化门脉高压患者胃黏膜组织VEGF表达增高。PHT胃黏膜淤血、缺氧与VEGF增加存在互动关系,VEGF在PHG发病过程中的作用可能是有限的。     

肝硬化患者胃黏膜前列腺素E2的研究

目的研究肝硬化患者胃黏膜前列腺素E2(PGE2)及意义。方法选取肝硬化患者60例及慢性胃炎、非溃疡性消化不良(NUD)患者各80例,行上消化道内镜检查,取胃窦及胃体各1块黏膜组织,用RIA法检测PGE2含量。结果(1)肝硬化组胃黏膜PGE2含量明显低于慢性胃炎及NUD组。(2)在肝硬化患者中,胃黏膜PGE2含量门脉高压胃病(PHG)组明显低于非PHG组,肝源性溃疡(HU)组亦明显低于非HU组,而与肝功能分级无关。结论(1)肝硬化胃黏膜防御机制减弱。(2)肝硬化胃黏膜PGE2的异常参与PHG及HU的形成。     

肝硬化患者胃黏膜表皮生长因子的研究

肝硬化患者常常并发门静脉高压性胃病（PHG）和肝源性溃疡（HU），但有关PHG及HU的发病机制，目前尚不十分清楚。表皮生长因子（EGF）是胃黏膜重要的保护因子，对其在肝硬化患者胃黏膜的含量以及与PHG、HU的关系研究，目前报道甚少。故我们对60例肝硬化患者胃黏膜EGF含量进行了检测，现报告如下。     

门脉高压性胃病患者一氧化氮和内皮素的变化及影响

目的探讨门脉高压性胃病(PHG)患者一氧化氮(NO)和内皮素(ET)含量的变化以及对临床的影响方法前瞻性随机对PHG29例和慢性胃炎(CG)32例患者采用硝酸还原酶法测定空腹血清NO含量,放射免疫分析法测空腹血浆ET含量.内镜检查时取胃粘膜,采用免疫组织化学技术显示诱导型一氧化氮合酶(iNOS)、结构型一氧化氮合酶(cNOS)的变化.结果①PHG组血清NO含量289.06μmol/L±140.19mool/L较CG组169.69μmol/L±56.29μm01/L明显增高,t检验,t=3.9398(P<0.05).②胃粘膜iNOS,cNOS阳性表达均较CG组高,两样本比较的秩和检验U=2.20088(P<0.05).③PHG组血浆ET含量7.44pg/mL±5.50pg/mL较CG组17.94pg/mL±8.05pg/mL明显降低,t检验t=6.2196(P<0.05);NO与ET含量做直线相关分析r=0.3601(P>0.05).④重型PHG血清NO含量较轻型增高,ET也较轻型增高,但差异均未达显著性(P>0.05).PHG轻重两型与Child-Pugh肝功能分级无关,与食管静脉曲张程度密切相关,计数资料相关分析x2=18.7854(P<0.0001).结论血NO升高在PHG的发生发展中起重要作用,胃粘膜iNOS,cNOS活性增高是血中一氧化氮升高的重要来源.低水平血浆ET含量对门脉高压的高动力循环起维持作用.     

门静脉高压性胃病与幽门螺杆菌感染血清一氧化氮内皮素水平关系的探讨

目的　探讨门静脉高压性胃病 (PHG)与食管静脉曲张分度、肝硬化病因、幽门螺杆菌 (H·pylori)感染、门静脉主干与脾静脉宽度、血清一氧化氮 (NO)、内皮素 (ET)水平关系。方法　对住院确诊的 137例肝硬化患者进行胃镜和彩色B超检查 ,同时检测患者血清NO、ET水平。结果　PHG的发生率为 35 6 % ,PHG患者血清NO、ET显著高于无PHG肝硬化患者 (P <0 0 1) ,PHG的发生率及其严重程度与食管静脉曲张程度、门静脉主干和脾静脉内径成正比。在ChildA、B、C级肝功能之间、不同病因肝硬化之间、是否感染H·pylori之间PHG的发生率差异均无显著意义 (P >0 0 5 )。结论　PHG的发生与肝硬化病因、肝功能和H·pylori感染关系不明显 ;NO、ET参与了门脉高压形成与PHG的发生与发展的机制。     

辛伐他汀对大鼠门脉高压性胃病的作用

目的探讨辛伐他汀在大鼠门脉高压性胃病(portal hypertensive gastropathy,PHG)中的作用与机制。方法采用门静脉主干部分结扎+左肾上腺静脉结扎法构建PHG模型。40只健康雄性Wistar大鼠随机分为假手术组(SO组,n=14)、模型组(LIG组,n=14)、辛伐他汀治疗组(SVS组,n=12)。于结扎2周后开始对SVS组大鼠予以辛伐他汀(20 mg/kg)灌胃,同时SO组和LIG组给予等量的生理盐水,1次/d,持续4周。4周后测量各组大鼠门静脉压力(portal pressure,PP)值,胃黏膜组织病理学变化、胃黏膜下层血管面积、血管最大直径及黏膜组织内诱导型一氧化氮合酶(inducible nitric oxide synthase,i NOS)、组织型一氧化氮合酶(constitutive nitric oxide synthase,c NOS)活性和NO含量。结果 LIG组大鼠胃黏膜病变严重,PP值、胃黏膜下层血管面积、血管最大直径、黏膜组织内i NOS活性及NO含量明显高于SO组(P0.01),c NOS和i NOS活性相对比例失衡。SVS组胃黏膜病变程度较LIG组明显减轻,PP值、胃黏膜下层血管面积、血管最大直径、黏膜组织内i NOS活性及NO含量明显低于LIG组(P0.01),但仍高于SO组(P0.01),c NOS和i NOS活性比例失衡在一定程度上得到纠正。结论辛伐他汀对PHG模型大鼠胃黏膜有保护作用,可能与降低胃黏膜组织内i NOS的活性、减少NO的过度产生、恢复i NOS与c NOS活性相对平衡有关。     

门脉高压性胃病患者胃黏膜中ET-1与HIF-1的表达及其意义

目的 探讨门脉高压性胃病(PHG)患者胃黏膜中内皮素-1(ET-1)和缺氧诱导因子-1(HIF-1)的表达及其相关性,为PHG的发病机制提供一定理论依据.方法 随机选择从2010年11月至2011年6月期间的PHG患者60例、门静脉高压症(PHT)无PHG患者30例和正常对照者20例,PHG组中分为轻型34例、重型26...     

血红素加氧酶-1在门静脉高压性胃病患者胃黏膜的表达

目的 探讨血红素加氧酶-1(HO-1)在肝硬化门静脉高压性胃病(PHG)患者胃黏膜的表达情况及其意义.方法 分别采集22例正常受试者(对照组)、20例门静脉高压(PHT)患者(PHT组)和22例PHG患者(PHG组)的胃黏膜标本,观察胃黏膜组织学变化,测定门静脉血流量(PVF).应用免疫组织化学法和Western blot方法检测HO-1蛋白在胃黏膜组织的表达情况,并分析HO-1蛋白与PVF、内镜下PHG严重程度的相关性,以及内镜下PHG严重程度与临床参数的相关性.结果 PHG组和PHT组患者胃黏膜中HO-1蛋白表达明显高于对照组(P＜0.05),而PHG组与PHT组之间比较差异无统计学意义(P＞0.05).PHG患者胃组织HO-1蛋白表达与内镜下PHG严重程度积分呈显著正相关(r =0.459,P＜0.05).内镜下PHG严重程度积分与食管静脉曲张程度(r=0.059,P＞0.05)、Child-Pugh分级(r=-0.001,P＞0.05)均无显著性相关.PHG组与PHT组患者的胃黏膜组织HO-1蛋白表达与PVF无显著性相关(r=0.071,P＞0.05).结论 HO-1蛋白在PHG患者胃黏膜中呈高表达,参与了PHG患者胃黏膜血液循环紊乱的发生.     

疏肝活血健脾方对门脉高压性胃病大鼠血清一氧化氮水平影响及防治作用研究

目的:运用一期门静脉缩窄法制备门脉高压性胃病(PHG)动物模型,从血清一氧化氮(NO)水平研究疏肝活血健脾方对PHG大鼠的防治作用.方法:选择健康雄性wistar大鼠120只,随机分为中药预防组(A)、中药大剂量组(B)、中药小剂量组(C)、西药对照组(D)、模型组(E)、模型生理盐水组(F)、空白对照组(G)和空白生理盐水组(H)共8组.采用一期门静脉缩窄法制备PHG动物模型.按要求造模灌胃后,在预定时间取大鼠眼球血,离心后取血清用硝酸还原酶法检测NO值.结果:A组大鼠血清NO值较F组明显降低,差异有非常显著性意义(P0.01);B组、C组、D组大鼠血清NO值较E组明显降低,两组比较差异有非常显著性意义(P0.01);B组疗效优于D组(P0.05)。结论:NO在PHG的发病机理中起着重要作用,疏肝活血健脾方能降低PHG大鼠NO水平,对PHG的防治效果肯定。     

重型颅脑损伤患者脑水肿指数与应激性消化道出血及血清NO和LPO水平的关系

目的探讨重型颅脑损伤患者脑水肿指数与应激性消化道出血以及血清一氧化氮(NO)和脂质过氧化物(LPO)水平的关系。方法选取2013年1月至2014年12月该院收治的重型颅脑损伤660例,其中并发应激性消化道出血患者80例,采用脑CT与颅内压在入院第2天和第5天监测患者的脑水肿指数,同时期监测患者血清中NO和LOP水平。结果脑水肿指数越高,患者消化道出血的发生率越高,出血量越大,持续时间约长(P0.05);入院第2天,各脑水肿指数患者血清中NO和LPO水平比较无统计学意义(P0.05),入院第5天,脑水肿指数越高,患者血清中NO和LPO水平也越高(P0.05)。结论重型颅脑损伤患者脑水肿指数越高,应激性消化道出血的发生率越高,且血清中NO和LOP水平也越高。     

肝硬化门脉高压性胃病患者胃粘膜炎症与一氧化氮合酶表达

目的 定位、定量研究肝硬化门脉高压性胃症（ＰＨＧ）患者胃粘膜炎症及其与一氧化氮合酶（ｉＮＯＳ／ｃＮＯＳ）表达的关系。方法 肝硬化患者６０例,其中伴有ＰＨＧ者３５例,无胃粘膜病变者２５例。胃粘膜活检３块,Ｂｏｕｉｎ固定,ＨＥ染色及免疫组化ＳＰ法ＭＰＶ显微分光光度计测定ｉＮＯＳ／ｃＮＯＳ表达。结果 肝硬化ＰＨＧ发生率５８．２％,其中７１．４％患者伴有胃粘膜炎症（Ｐ〈０．０５）;胃粘膜炎症者胃粘膜血管ｉ     

一氧化氮和前列腺素在门静脉高压性胃病大鼠胃粘膜灌注中的作用

目的 探讨一氧化氮（NO）和前列腺素在门静脉高压性胃病（PHG）大鼠胃粘膜灌注中的作用。方法 部分结扎大鼠门静脉主干2周后,采用中性红清除率法测定大鼠胃粘膜血流量（GMBF）,同时观察门静脉压力（PVP）的变化。结果 PHG组大鼠GMBF和PVP显著高于假手术组（t=3.431、3．312,P＜0．01）。低剂量的NO合成酶抑制剂L－硝基－精氨酸甲酯（L－NAME）呈剂量依赖性降低PHG大鼠GMBF,而对假手术组GMBF无明显影响;高剂量的L－NAME（12mg/kg)能非常显著降低PHG和假手术组大鼠GMBF。前列腺素环氧合酶抑制剂消炎痛能明显降低PHG组大鼠GMBF,而对假手术组GMBF无明显影响;预先给消炎痛处理后在假手术组大鼠中,静脉注射低剂量L－NAME（4mg/kg)前后GMBF无明显变化,高剂量L－NAME（12mg/kg)降低大鼠的GMBF与未用消炎痛处理组比无明显变化;预先给消炎痛处理后在PHG组大鼠中,L－NAME剂量（4mg/kg、12mg/kg)依赖性降低大鼠的GMBF与未用消炎痛处理组比无明显改变。结论 NO、前列腺素在调节PHG大鼠的GMBF起重要作用,但两者无协同作用。     

善得定对门静脉高压性胃病大鼠胃粘膜灌注的影响

目的 观察善得定对门静脉高压性胃病（ｐｏｒｔａｌ ｈｙｐｅｒｔｅｎｓｉｖｅ ｇａｓｔｏｐａｔｈｙ,ＰＨＧ）大鼠胃粘膜血流最（ｇａｓｔｒｉｃ ｍｕｃｏｓａｌ ｂｌｏｏｄ ｆｏｗ,ＧＭＢＦ）的影响,并对其作用机制作初步探讨。方法 部分结扎大鼠门静脉主干２周后,观察善得定对ＰＨＧ大鼠全身血流动力学,ＧＭＢＦ,门静脉压力（ＰＶＰ）的影响,测定了输注善得定３０ｍｉｎ后ＰＨＧ大鼠血浆胰高糖素,血浆和胃粘膜ＮＯ     

The effects of transjugular intrahepatic portosystemic shunt on portal hypertensive gastropathy

In addition to variceal bleeding, haematemesis may occur due to haemorrhagic gastritis in patients with portal hypertension. This has been known as portal hypertensive gastropathy (PHG). We have evaluated the effects of the transjugular intrahepatic portosystemic shunt (TIPS) on portal venous pressure (PVP) and endoscopic gastric mucosal changes observed in patients with portal hypertension. We performed TIPS in 12 patients with complications due to portal hypertension as follows: variceal bleeding in nine patients (bleeding from oesophageal varices in seven and gastric varices in two), refractory ascites in three and haemorrhage from severe PHG in one. Endoscopic examinations were performed before and after TIPS for all patients. Changes of PVP and gastric mucosal findings on endoscopy were analysed. Before TIPS, PHG was seen in 10 patients. Portal venous pressure decreased from an average of 25.1 ± 8.8 to 17.1 ± 6.2 mmHg after TIPS ( P < 0.005). On endoscopy, PHG improved in nine of 10 patients. Oesophagogastric varices improved in eight of 11 patients. In one patient with massive haematemesis, haemorrhage from severe PHG completely stopped after TIPS. Because TIPS effectively reduced PVP, this procedure appeared to be effective for the treatment of uncontrollable PHG.     

Role of endothelin-1 in congestive gastropathy in portal hypertensive rats

BACKGROUND: The aim of this study was to determine the role of endothelin (ET)-1 in portal hypertensive gastropathy (PHG) under portal hypertension, in order to investigate whether the ET(A/B) receptor inhibitor improves the permeability of gastric mucosal microvessels in PHG. METHODS AND RESULTS: Portal hypertensive rats (PVL) and sham-operated rats (CTR) were prepared and then the concentration of plasma ET-1 was measured and the vasopressor response to ET-1 was compared between the two groups. The plasma ET-1 levels in PVL increased significantly compared with CTR; however, the vasopressor response to ET-1 in PVL decreased more than in CTR. Next, the portal venous pressure was measured in both CTR and PVL pretreated with or without a nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), before the injection of ET-1. The portal venous pressure of PVL after receiving ET-1 and being pretreated with L-NAME significantly increased in comparison to the pressure of PVL treated with ET-1 alone (without L-NAME). Moreover, Evans-Blue was injected into each rat and the absorbancy of the gastric contents was measured. The absorbancy of Evans-Blue in PVL increased significantly compared with CTR; however, the absorbancy in PVL+ ET(A/B) receptor inhibitor (Ro47-0203) decreased significantly more than in PVL. CONCLUSIONS: This study showed that ET-1 is a potent vasoconstrictive substance that also has a transitory vasodilative response through NO induced by ET-1 in portal hypertension. In addition, it was found that the vascular permeability of the gastric mucosa increased in portal hypertension and that Ro47-0203 inhibited the hyper-permeability. Accordingly, ET-1 may, thus, play an important role in the development of PHG through NO induced by ET-1. Ro47-0203 may, therefore, be a useful substance for improving PHG in portal hypertension.     

门脉高压性胃病与幽门螺杆菌感染的关系

目的探讨门脉高压性胃病（ｐｏｒｔａｌｈｙｐｅｒｔｅｎｓｉｖｅｇａｓｔｒｏｐａｔｈｙ，ＰＨＧ）与幽门螺杆菌（Ｈｅｌｉｃｏｂａｃｔｅｒｐｙｌｏｒｉ，Ｈｐ）感染之间的关系．方法ＰＨＧ患者６８例，通过内镜检查诊断，胃粘膜活检（每例４块）用Ｗａｒｔｈｉｎ＿Ｓｔａｒｒｙ银染色法检测Ｈｐ．结果ＰＨＧ患者的Ｈｐ阳性率为６０３％（４１／６８），合并消化性溃疡的ＰＨＧ患者Ｈｐ阳性率为５３７％（２２／４１），单纯性ＰＨＧ患者Ｈｐ阳性率为４６３％（１９／４１）．结论ＰＨＧ患者的胃粘膜病变与Ｈｐ感染有密切关系     

Zinc L-carnosine protects against mucosal injury in portal hypertensive gastropathy through induction of heat shock protein 72

BACKGROUND AND AIMS: Increased susceptibility to gastric mucosal injury is observed in portal hypertensive gastropathy (PHG). In this study, the effects of zinc L-carnosine, an anti-ulcer drug, were evaluated on expression of heat shock protein (hsp) 72 and cytoprotection in gastric mucosa in a rat model of PHG. METHODS: Portal hypertensive gastropathy with liver cirrhosis was induced by bile duct ligation for 4 weeks in male Sprague-Dawley rats. Expression of gastric mucosal hsp72 was evaluated by Western blotting at 6 h after intragastric administration of L-carnosine, zinc sulfate, or zinc L-carnosine. Blood was also collected for determination of serum zinc level. Mucosal protective abilities against hydrochloric acid (HCl) (0.6N) followed by pretreatment with L-carnosine, zinc sulfate or zinc L-carnosine were also studied. RESULTS: L-carnosine, zinc sulfate, and zinc L-carnosine induced hsp72 in gastric mucosa of rats with bile duct ligation. Zinc sulfate and zinc L-carnosine suppressed HCl-induced mucosal injury. However, L-carnosine could not suppress HCl-induced mucosal injury. Serum zinc levels were significantly elevated after zinc L-carnosine administration. Furthermore, pretreatment with zinc L-carnosine (30-300 mg/kg) increased the expression of hsp72 in gastric mucosa and prevented HCl-induced mucosal injury in rats with bile duct ligation in a dose-dependent manner. CONCLUSIONS: Zinc derivatives, especially zinc L-carnosine, protected portal hypertensive gastric mucosa with increased hsp72 expression in cirrhotic rats. It is postulated that zinc L-carnosine may be beneficial to the mucosal protection in PHG as a 'chaperone inducer'.     

Role of vasoactive intestinal peptide and nitric oxide in the modulation of electroacupucture on gastric motility in stressed rats

INTRODUCTION In recent years, along with the extensive research into enteric nerve system (ENS), increasing evidence shows that peptidergic neurotransmitters are the key factors regulating the gastric motility. Our previous research[1-3] showed that electroacupucture (EA) at acupoints of the Stomach Meridian of Foot-Yangmin may regulate gastric movement, increase blood flow in the microvessels in the gastric mucosa, and exert a protective effect on gastric mucosa. Nitric oxide (NO) an…     

Effects of propranolol on gastric mucosal perfusion and serum gastrin level in cirrhotic patients with portal hypertensive gastropathy

Gastric mucosal hyperemia associated with elevated serum gastrin level has been suggested in cirrhotic patients with portal hypertensive gastropathy (PHG). Clinical evidence has shown that these patients may benefit from propranolol administration. The aim of this study was to investigate effect of propranolol on gastric mucosal perfusion and serum gastrin level in cirrhotic patients with portal hypertensive gastropathy. Gastric mucosal perfusion was assessed by laser Doppler flowmetry. Measurements were performed under basal conditions and after observer-blind administration of propranolol (30–60 mg/day,N=9) or placebo (N=9) for seven days. Placebo had no effect on either gastric mucosal perfusion or serum gastrin level. In contrast, propranolol administration significantly decreased both antrum gastric mucosal perfusion (from 0.88±0.28 to 0.73±0.26 V,P<0.05) and corpus gastric mucosal perfusion (from 0.94±0.35 to 0.78±0.25 V,P<0.05). However, this drug had no effect on serum gastrin level. We conclude that chronic propranolol administration in cirrhotic patients with portal hypertensive gastropathy may reduce gastric mucosal perfusion without changing serum gastrin level.