丹对门脉高压大鼠胃粘膜及肝脏的影响

用丹参对肝硬变门脉高压大鼠进行了治疗，并与心得它进行了比较，结果表明，丹参和心得安均可使门脉压力下降，胃粘膜前列腺素Ｅ２含量，胃粘膜血流量和胃壁结合粘液量增加，但心得安使肝细胞坏死加重，血清ＡＬＴ和ＴＢ不能降低，ＡＬＴ反有升高，而丹参可使肝细胞损害减轻，肝内纤维组织减少，ＡＬＴ，ＡＬＰ和ＴＢ降至正常水平，说明心得安虽可使门脉压性胃粘膜病变改善，却可加重肝损害，而丹参不仅可使胃粘膜病变改善，而且还能     

汉防己甲素对肝硬化门脉高压大鼠胃粘膜及肝脏的影响

为探讨汉防己甲素对门脉高压性胃粘膜病变的治疗作用，观察了汉防己甲素对门脉高压大鼠门脉压力、胃粘膜屏障功能、肝脏组织学和肝功能的影响，并与普萘洛尔进行了对比。结果表明，汉防己甲素和普萘洛尔均可使门脉高压大鼠的ＰＶＰ下降，胃粘膜ＰＧＥ２含量、ＧＭＢＦ和ＧＡＭ增加。但普萘洛尔使肝细胞坏死增加，ＡＬＴ和ＳＴＢ不能降低，ＡＬＰ反有升高。而汉防己甲素则使肝细胞损害减轻，肝内纤维组织减少，ＡＬＴ、ＡＬＰ和ＳＴＢ降至正常水平。提示，普萘洛尔虽可使ＰＨＴ性ＧＭＬ改善，却可加重肝损害。而汉防己甲素不仅可改善胃粘膜屏障功能，而且还能改善肝功能。     

血清谷氨酰转肽酶在慢性乙型肝炎诊断中的价值

目的 探讨血清γ－谷氨酰转肽酶（ＧＧＴ）在慢性乙型肝炎（ＣＨＢ）不同程度肝脏病理损害中的变化规律及其在ＣＨＢ诊断中的价值。方法 测定２２１例ＣＨＢ患者血清ＡＬＴ、ＡＳＴ及ＧＧＴ水平，同时行肝活体组织检查，对肝组织进行炎症分级和纤维分期。分析ＡＬＴ、ＡＳＴ、ＧＧＴ与ＣＨＢ之间的关系。结果 （１）病理轻度和重度ＣＨＢ的ＧＧＴ正常率分别为９０．４％和１２３％（Ｐ＜００１）；（２）临床诊断为轻度、而病理诊断分别为轻、中、重度的ＣＨＢ患者中，ＧＧＴ依次递升（Ｐ＜０．０１）；（３）在活动性ＣＨＢＳ患者中，ＧＧＴ随ＡＬＴ的升高而升高，存在着正向线性相关（ｒ＝０．４６４；Ｐ＜０．００１）。在保肝治疗中，ＧＧＴ、ＡＬＴ较快降至正常的为轻度ＣＨＢ；ＧＧＴ持续在一个较高水平波动，而ＡＬＴ下降，甚至呈ＡＬＴ－ＧＧＴ分离的多分别为中或重度ＣＨＢ。结论ＧＧＴ是提高ＣＨＢ临床与病理诊断符会率的一个有价值的参考指标。     

诱导型一氧化氮合酶在ConA诱发T细胞介导的小鼠肝损害中的表达

目的观察诱导型一氧化氮合酶（ｉＮＯＳ）在刀豆素Ａ（ＣｏｎＡ）诱发Ｔ细胞介导的小鼠肝损害中的表达及意义。方法应用黄递酶染色（ＮＡＤＰＨ－ｄ）技术观察ｉＮＯＳ表达。结果ＣｏｎＡ造成肝损害后，血浆中亚硝酸盐（ＮＯ－２）较正常对照组（ＰＢＳ组）显著升高，以Ｌ－ＮＡＭＥ抑制ＮＯ合成，肝细胞损害反而加重，且肝组织内丙二醛（ＭＤＡ）增加，肝窦内血细胞聚集加重；在ＣｏｎＡ造成肝损害时可见肝实质细胞表达ｉＮＯＳ，且越靠近中央静脉的肝细胞表达越多，推测这是肝细胞对缺血缺氧而产生的一种自身反映；用环孢霉素Ａ（ＣＳＡ）预先抑制Ｔ细胞活化，则未发现肝细胞表达ｉＮＯＳ。结论在ＣｏｎＡ性肝损害中，肝实质细胞通过启动自身的ＮＯ生物合成机制参与了炎症应答，并通过消除氧自由基和抑制血细胞在肝窦内聚集而起一定的保护作用，这一生物过程很可能是肝细胞参与机体免疫应答的一部分。     

丹参、心得安对门静脉高压症大鼠门静脉压力和胃肠激素的影响

目的:观察丹参、心得安对门脉高压症大鼠门静脉压力、胃肠激素的影响.方法:采用CCl4加酒精饮料制作大鼠门脉高压模型,造模4周后分别给大鼠服用丹参、心得安,造模结束后用Medlab-Ug4Cs生物信号采集处理系统检测正常组、模型组、丹参治疗组、心得安治疗组大鼠门静脉压力.处死大鼠后颈动脉取血,用放免法检测4组大鼠血浆胃肠激素(胃动素、胃泌素、胰高血糖素)的含量.结果:模型组大鼠门静脉压力较正常组明显升高(P＜0.01),丹参治疗组、心得安治疗组大鼠门脉压力较模型组明显下降(P＜0.01),丹参治疗组大鼠门脉压力与心得安治疗组比较差异无显著性意义(P＞0.05).心得安组大鼠与模型组比较胃动素含量无明显改善(P＞0.05),而胃泌素、胰高血糖素明显下降(P＜0.05).丹参治疗组大鼠胃泌素、胃动素、胰高血糖素含量与模型组比较明显下降(P＜0.01或P＜0.05),与心得安治疗组比较,胃动素、胰高血糖素指标下降明显(P＜0.05).结论:丹参能有效降低门脉高压症大鼠门静脉压力,调节胃肠激素,疗效优于心得安治疗组.其作用机制可能与其良好的抗肝纤维化、阻止肝硬化形成、调节胃肠激素水平、改善肝功能等作用有关.     

丹参对门脉高压血流动力学影响的实验与临床研究

为研究丹参对肝硬化门脉血流动力学的影响，利用血管插管测定用药前后胆管结扎肝硬化犬门脉系统压力变化，超声多普勒监测肝硬化患者用药后门静脉系统血流动力的改变。结果：（１）丹参静脉给药可使肝硬化犬门静脉压（ＰＰＶ）、嵌塞肝静脉压（ＷＨＶＰ）、肝静脉压力梯度（ＨＶＰＧ）显著降低（Ｐ＜０．０５～０．０１），而平均动脉压（ＭＡＰ）、心率（ＨＲ）无明显变化（Ｐ＞０．０５）；（２）丹参长期口服（１０～１２周），可显著降低肝硬化患者（Ｃｈｉｌｄ－ＰｕｇｈＡ、Ｂ级）门静脉内径（ＤＰＶ）、脾静脉内径（ＤＳＶ）、门静脉血流量（ＱＰＶ）、脾静脉血流量（ＱＳＶ）（Ｐ＜０．０５～０．０１），并对患者乏力、厌食、腹胀及肝功能（ＡＬＴ）具有部分改善作用，未见副作用。本研究表明，丹参为安全有效的降低门静脉压力药物，值得对其做进一步研究。     

肝硬化门脉高压症的病因与发病机理

引起门脉高压症的原因很多,慢性进行性弥漫肝细胞损害形成的实性及窦后性门脉高压症即为肝硬化门脉高压症。病毒、酒精物质、化学、药物等导致弥漫性肝细胞变性坏死,伴随出现肝内纤维组织增生及肝细胞再生结节使肝内微循环阻力增加及内脏高动力循环,是我国肝硬化门脉高压症的最常见原因。广义来讲,肝内、外门脉系及肝静脉、胆管系弥漫阻塞或大枝阻塞及炎症,反复且长期存在亦可造成肝硬化门脉高压症。     

门脉高压时的胃粘膜病变

门脉高压病人的胃粘膜具独特的形态学和功能改变,对应激或外来侵袭因素的敏感性增高,易并发上消化道出血。用传统的制酸、消炎药物治疗往往失败,而采用降低门脉压力的疗法如服用心得安,则常能奏效。目前有人主张将合并于门脉高压的胃粘膜病变称为“充血性胃病”。     

151例抗结核药物性肝损害分析

肝损害是影响结核病治疗顺利进行的重要因素。本文对我院三年来１５１例肝损害病例进行分析,以探讨对抗结核药物性肝损害的对策。１临床资料１．１１５１例肝损害中男性１１３例、女性３８例,年龄１９～８４岁,平均４６岁,大于６０岁３８例占２５％（３８／１５１）。依照肝损害程度分为轻、中、重三等级。轻度肝损害指ＡＬＴ、ＡＳＴ值＜２×正常上限ＵＬＮ,中度肝损害指ＡＬＴ、ＡＳＴ＞２×ＵＬＮ伴一项其它指标异常或有症状及体征,重度肝损害指ＡＬＴ、ＡＳＴ、ＴＢＩＬ、γ－ＧＴ、ＴＰ等多项指标异常伴有症状／或体征如食欲下降…     

血清总胆汁酸测定对急性、慢性肝炎诊断的价值

目的 探讨急性、慢性肝炎血清总胆汁酸（ＴＢＡ）测定的可能作用。方法 经肝穿刺活检病理证实为急性、慢性病毒性肝炎９２例，对ＴＢＡ含量进行了测定，并与ＡＬＴ及ＴＢｂｉｌ进行对比分析。结果 急性肝炎与慢性肝炎ＴＢＡ与正常组比较有显著性差异（Ｐ均〈０．００１），慢性肝炎轻、中、重型三组ＴＡＢＡ经Ｘ＾２和t检验，各组生差异（Ｐ〉 ０．０５）。结论 急性肝炎时ＴＢＡ检测与ＡＬＴ同样具有高度为敏性，在慢性肝炎ＴＢ     

Effects of tetrandrine on gastric mucosa and liver in portal hypertensive rats

ＥｆｅｃｔｓｏｆｔｅｔｒａｎｄｒｉｎｅｏｎｇａｓｔｒｉｃｍｕｃｏｓａａｎｄｌｉｖｅｒｉｎｐｏｒｔａｌｈｙｐｅｒｔｅｎｓｉｖｅｒａｔｓＭＵＹｉ，ＳＨＥＮＹａｏＺｏｎｇａｎｄＣＨＵＹｉＦａｎｇＳｕｂｊｅｃｔｈｅａｄｉｎｇｓｌｉｖｅｒｇａｓｔｒｉｃｍ...     

Propranolol reduces ethanol-induced gastric mucosal damage in portal hypertensive rats

In a standardized rat model of portal hypertension, we investigated the effects of propranolol on alcohol-induced gastric mucosal damage. Portal hypertensive rats pretreated with 2 mg propranolol, compared with those receiving saline, had significantly reduced portal pressures (24 +/- 1 vs 32 +/- 1 cm saline), macroscopic mucosal damage (24 +/- 1 vs 39 +/- 4% of mucosa), and histologic deep necrosis (36 +/- 2 vs 61 +/- 4% of mucosal length). Increased dosage of propranolol to 4 mg did not produce any further reduction of portal pressure or mucosal damage. Central venous and systemic arterial pressures were not significantly altered by propranolol. The extent of mucosal damage correlated with levels of portal pressure (P less than 0.01) in portal hypertensive rats. Sham-operated normotensive rats had less macroscopic mucosal damage (26 +/- 4%) than portal hypertensive rats, and propranolol did not affect the extent of ethanol-induced damage or portal pressures in these animals. We conclude: (1) Propranolol is effective in reducing extent of ethanol-induced gastric mucosal damage in portal hypertensive rats, but not in sham-operated controls; (2) this effect correlates with reduction of portal pressure; and (3) our study supports the clinical impression that reducing portal pressure may be one approach for the prevention and therapy of gastric mucosal damage in portal hypertension.     

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.     

Effects of propranolol and sucralfate on ethanol-induced gastric mucosal damage in chronic portal hypertensive rats

In a rat model of chronic portal hypertension we studied ethanol-induced gastric mucosal damage and the effects of pretreatment by propranolol and sucralfate. Susceptibility to ethanol was increased in chronic portal hypertensive rats compared with sham-operated rats (55 +/- 8% vs. 25 +/- 4%). Both acute pretreatment (10 min) and chronic pretreatment (3 weeks) with propranolol reduced gastric mucosal injury induced by ethanol in portal hypertensive rats, compared with saline-treated rats. Acute and chronic pretreatment with propranolol had no protective effect in sham-operated rats. In portal hypertensive rats, sucralfate in two different doses (500 and 125 mg/kg) protected the gastric mucosa against ethanol-induced gastric injury compared with animals receiving saline (2 +/- 1% and 3 +/- 2% vs. 25 +/- 3%). Sucralfate at the higher dose did not reduce portal pressure in portal hypertensive rats. We conclude that: (1) chronic portal hypertension increases ethanol-induced gastric damage; (2) acute and chronic propranolol treatment reduces ethanol-induced gastric injury in portal hypertensive rats, probably by decreasing portal hypertension; (3) sucralfate has a cytoprotective effect in portal hypertensive rats without reducing portal pressure. These results suggest a potential application of sucralfate in patients otherwise treated by sclerotherapy.     

Does portal hypertension contribute to the pathogenesis of gastric ulcer associated with liver cirrhosis?

The prevalence of gastric ulcers in patients with liver cirrhosis is increased compared with that in the general population, and portal hypertension may contribute to the increased risk of gastric ulcer in cirrhosis patients. Aggressive factors involved in the pathogenesis of gastric ulcer are diminished in association with portal hypertension. In contrast, most of the important gastric mucosal defense mechanisms are shown to be impaired in portal hypertension; many of these mechanisms are also found to be altered in patients with liver cirrhosis. Portal hypotensive treatment with propranolol reduces ethanol-induced gastric mucosal damage in portal hypertensive rats and improves endoscopic signs of portal hypertensive gastropathy in cirrhosis patients. Together, these findings suggest portal hypertension-induced impairment of the gastric mucosal defenses to be an important factor in the pathogenesis of gastric ulcer in patients with liver cirrhosis. Prospective studies of portal pressure-reducing procedures, such as pharmacotherapy with propranolol, and their effect on the incidence of gastric ulcer in cirrhosis patients are needed to confirm this suggestion.     

Effect of early propranolol administration on portal hypertensive gastropathy in cirrhotic rats

AIM： To investigate any protective effect of early propranolol administration in the development of portal hypertensive gastropathy in cirrhotic rats. METHODS： For the development of liver cirrhosis and portal hypertensive gastropathy, 60 rats underwent ligation of the left adrenal vein and complete devascularization of the left renal vein, followed by phenobarbital and carbon tetrachloride （CCl4） administration. After two weeks of CCl4 administration, the rats were randomly separated into two groups. In group A, propranolol was continuously administered intragastrically throughout the study, whereas in group B normal saline （placebo） was administered instead. Hemodynamic studies and vascular morphometric analysis of gastric sections were performed after complete induction of cirrhosis. RESULTS： Vascular morphometric studies showed higher numbers of vessels in all mucosal layers in the control group. Statistical analysis revealed a significantly higher total vascular surface in the control group compared to the propranolol group, but with no statistically significant difference between the mean vascular surfaces between the groups. Our study clearly shows that the increased mucosal blood flow is manifested by a marked increase of vessel count. CONCLUSION： Early propranolol＇s administration in portal hypertensive cirrhotic rats seems to prevent intense gastric vascular congestion that characterizes portal hypertensive gastropathy.     

Effects of octreotide and propranolol on colonic mucosa in rats with portal hypertensive colopathy

BACKGROUND/AIMS: The aim of the study is to clarify the effects of octreotide and propranolol, agents used in the treatment of portal hypertension, on mucosal changes in portal hypertensive colopathy. METHODOLOGY: Portal hypertension was induced in all rats by partial portal vein ligation, and after the operation all rats were caged for a 10-week period. Then, animals were divided into three groups and for two weeks medical treatment were administered to the individual groups as follows: Control group, saline 0.5 mL/day, intraperitoneally. Octreotide group, octreotide 100 micrograms/kg/12 hours, subcutaneously. Propranolol group, propranolol 20 mg/kg/day, intraperitoneally. In order to assess the portal hypertensive colopathy, criteria such as mean diameters of dilated vessels in colonic mucosa, and the existence of mucosal edema, capillary ectasia, hyperemia and hemorrhage, inflammation were used. RESULTS: When parameters were compared for the control versus propranolol groups, mucosal edema and hyperemia and hemorrhage criteria were found to be significant for the propranolol group; control versus octreotide groups, mucosal edema, capillary ectasia, and hyperemia and hemorrhage criteria were found to be significant for the octreotide group; octreotide versus propranolol groups, capillary ectasia and mucosal edema criteria were found to be significant for the octreotide group. CONCLUSIONS: The mucosal changes in portal hypertensive colopathy could be corrected by drugs modifying portal blood flow, octreotide may find a place in the treatment of portal hypertensive colopathy.     

Management of portal hypertension in children: a retrospective study with long-term follow-up

OBJECTIVES: Data regarding the management of the portal hypertensive haemorrhage in the paediatric patients have yielded conflicting results. The purpose of this study was to evaluate the efficacy of beta-blocker (propranolol) alone, sclerotherapy alone and beta-blocker + sclerotherapy combination in the management of portal hypertension in the paediatric population. METHODS: Medical information was retrieved from the records of 62 children with portal hypertension who were under treatment during at least two years of follow-up period. Data collected included diagnosis, type of portal hypertension, age at initiation of therapy, bleeding episodes before and during therapy. RESULTS: Sixteen of 62 patients were diagnosed as extrahepatic portal hypertension, 46 as intrahepatic portal hypertension. The mean age of study population was 7.6 +/- 4.2 years, 45 percent being females. The mean duration of follow-up under therapy was 5.2 +/- 2.5 years. Among the patients with intrahepatic portal hypertension, 29 received propranolol + sclerotherapy, 12 received only propranolol and 5 received only sclerotherapy. There was no significant decrease in bleeding episodes during propranolol or sclerotherapy. However patients under propranolol + sclerotherapy, showed significant decrease in bleeding episodes during therapy (23/29 before therapy, 15/29 during therapy, p < 0.05). Rebleeding index in patients with IHPH was significantly long in the group treated by propranolol + sclerotherapy (p = 0.0001) compared with before therapy. Because the numbers of patients in the groups are small, Kaplan Meier estimation suggest that propranol treatment is more effective. But there isn't significant difference when the results were compared with those of before therapy, except in the combined treatment group. CONCLUSION: The monotherapy is not sufficient for longterm follow-up of portal hypertensive patients. The combination therapy with propranolol + sclerotherapy appears more encouraging in the prevention of portal hypertensive haemorrhage, but this needs to be assessed in randomized trials.