肝硬化门脉高压症大鼠模型制作方法的探讨

目的：建立稳定可靠的肝硬化门脉高压大鼠动物模型。材料与方法：50只雄性sD大鼠,随机分为3组。正常对照组10只,行假手术,给予正常饮食。肝硬化A组20只,先行左肾上腺静脉结扎,然后给予初始浓度为0．03％的硫代乙酰胺（thioacetamide,TAA）溶液作为饮用水并根据大鼠体重变化调节给药浓度。肝硬化B组20只,行假手术,给予固定浓度为0．03％TAA溶液。给药时间为14周。结果：肝硬化A组大鼠死亡率为0,肝硬化形成率达到100％。肝硬化B组大鼠死亡率15％,肝硬化形成率75％。肝硬化A组大鼠的门静脉压力明显高于肝硬化B组和对照组。结论：采用左肾上腺静脉结扎并根据体重变化调节TAA给药浓度可建立稳定可靠的肝硬化门脉高压大鼠动物模型。     

急诊断流术在门静脉高压症并食道胃底静脉出血的疗效观察

目的观察急诊断流术在门静脉高压症并食道胃底静脉出血的临床疗效。方法选取我院收治的门静脉高压症并食道胃底静脉出血患者103例,随机分为两组。对照组52例,在患者入院后先采取保守止血治疗,再择期进行断流术;观察组51例,在患者入院后立即采取急诊断流术治疗。观察比较两组的临床疗效。结果观察组患者术后死亡率为11.76%,对照组为25.00%,两组比较差异有统计学意义(P0.05)。观察组患者住院时间短于对照组,差异有统计学意义(P0.05)。经随访3~4年,观察组再次出血发生率为12.76%,对照组再次出血发生率为13.46%,两组比较差异无统计学意义(P0.05)。结论急诊断流术在门静脉高压症并食道胃底静脉出血的临床疗效显著,可降低患者死亡率,缩短住院时间,值得临床应用。     

三株口服液对门脉高压症术后的疗效观察

三株口服液双歧杆菌是复合制剂,经６９例门脉高压症术后（断流术）病人口服１５ｄ－２８ｄ。治疗前后分别检测血内毒素含量及肝功能并观察其临床症状的改变。结果表明：本制剂对门脉高压病术后的疗效明显。总有效率为７９．８％,其中内毒素水平治疗后明显下降,与治疗前比较,Ｐ＜０．０５,有效率为８６．９５％。肝功能各项指标有不同程度的改善,有效率为７８．２６％,腹胀亦明显改善。     

内镜下硬化剂和套扎治疗食管静脉曲张术后对门脉高压性胃病和胃底静脉曲张的影响

目的:探讨食管静脉曲张(EV)采用内镜下套扎术(EVL)和硬化剂(EVS)治疗对患者近远期并发胃底静脉曲张(GV)以及门脉高压性胃病(PHG)并发症的影响。方法:抽选我院肝硬化上消化道出血后接受内镜下治疗的患者97例为研究对象,其中19例予以内镜下EVS治疗,78例行内镜下EVL治疗,随访1年,观察治疗3个月、6个月、1年后并发GV、PHG的近远期概率。结果:治疗3个月后,本组患者GV、PHG等并发症的发生率为17.5%(17/97)、39.2%(38/97),与治疗前比较差异无显著性(P0.05);治疗6个月后,本组患者GV、PHG等并发症的发生率为32%(31/97)、70.1%(68/97),与治疗前相比,并发人数显著增加(P0.05);治疗1年后,GV、PHG的发生率为42.3%(41/97)、88.7%(86/97),并发人数显著高于治疗前(P0.05)。结论:内镜下EVS、EVL治疗在消退食管曲张静脉和良好地控制出血的同时,还可增加PHG、GV的并发几率,值得临床重视预防。     

PTVE 与TIPS治疗肝硬化门静脉高压合并食管胃底静脉曲张破裂出血 的疗效比较

目的:研究经皮胃底曲张静脉栓塞术(PTVE)和经颈静脉肝内门体分流术(TIPS)治疗肝硬化门静脉高压合并食管胃底静脉曲张破裂出血的临床疗效,为临床治疗提供依据。方法:选取2001年4月到2015年4月我院肝硬化门静脉高压合并食管胃底静脉曲张破裂患者169例,根据手术方式分为PTVE组(行PTVE治疗)141例和TIPS组(行TIPS治疗)28例,比较两组术前、术后门静脉压力,术前、术后3个月、6个月以及1年两组Child-Pugh评分、白蛋白以及直接胆红素,并比较两组再出血和肝性脑病发生率。结果:TIPS组术后门静脉压力较术前显著降低,比较差异具有统计学意义(P0.05),术后PTVE组及TIPS组组间比较差异具有统计学意义(P0.05);两组术前和术后各时间直接胆红素无统计学意义(P0.05);PTVE组术后1年白蛋白水平显著升高,与术前和TIPS组比较差异具有统计学意义(P0.05),TIPS组术后白蛋白有所升高,但各时间比较差异无统计学意义(P0.05),PTVE组术后各时间Child-Pugh评分较术前明显改善,比较差异具有统计学意义(P0.05),TIPS组术后3个月和术后6个月Child-Pugh评分较术前明显改善,比较差异具有统计学意义(P0.05);两组术后再出血发生率比较无统计学意义(P0.05),PTVE组肝性脑病发生率显著低于TIPS组,比较差异具有统计学意义(P0.05)。结论:PTVE和TIPS治疗肝硬化门静脉高压合并食管胃底静脉曲张破裂出血效果相当,TIPS能显著降低门静脉压,PTVE能降低肝性脑病的发生率,改善患者Child-Pugh评分。     

左侧门脉高压症并上消化道出血的诊断与治疗（附14 例临床分析）

目的:探讨左侧门脉高压症合并上消化道出血的诊断和治疗方法。方法:回顾分析我院近10年来收治的14例左侧门脉高压症合并上消化道出血患者的诊治措施和随访结果。结果:14例患者均有呕血或(和)黑便史,无肝硬化、腹水及肝功能异常等表现。14例患者中胰体尾占位6例,胰腺假性囊肿4例,慢性胰腺炎4例。14例患者均采用手术治疗。9例患者获得随访,定期内镜复查,曲张静脉明显改善或消失,随访5月～8年均无再出血。结论:胰腺疾病病史、无肝硬化和肝功能正常、孤立性胃底静脉曲张和脾肿大及脾亢是诊断左侧门脉高压症的基本要点。该疾病可通过脾切除术或联合胃底周围血管离断术结合原发胰腺疾病的治疗来获得治愈。     

食管胃底静脉曲张出血药物治疗进展

在慢性肝病晚期患者中,门静脉高压属于普遍存在的并发痘之一。临床上门静脉高压往往会引发食管胃底静脉曲张,最终出现破裂出血。随着研究的进一步深入,目前研究证实肝脏结构出现改变、肌纤维母细胞发生收缩以及缩血管活性物质分泌的增加是引发门脉阻力上升最主要的三个方面。研究表明,门脉阻力上升能够被一些药物所阻断,这为临床使用一些缩血管药物降低门静脉高压,预防食管胃底静脉曲张出血（EVB）提供了理论基础。     

一氧化氮与肝硬化门脉高压高动力循环的关系

目的 :研究肝硬化门脉高压血清NO水平与血流动力学改变之间的关系。方法 :用比色法检测35例肝硬化病人和 2 5例正常人血清NO浓度 ,用彩色多普勒检测肝硬化组及正常组门静脉横径及门静脉血流量。结果 :肝硬化门脉高压患者血清NO显著升高。结论 :检测血清NO可作为判断肝硬化门脉高压的指标 ,血清NO在高动力循环中起重要作用     

心得安预防门脉高压引起初次消化道出血的疗效观察

目的:观察心得安预防门脉高压症消化道出血的疗效、不良反应及临床应用的注意事项。方法选择本院102例肝硬化食道胃底静脉曲张患者,随机分为心得安组(52例)和安慰剂组(25例)。对出血发作的病情、持续的时间、输血量的多少、对止血药物的反应、生存期以及副反应进行观察。结果随访12个月,治疗组出血发生率为19.2%,安慰剂组为28%,两组差异无显著意义。随访20个月,治疗组出血发生率28.8%,安慰剂组48%,两组比较有显著性差异(P<0.05),但生存时间无显著差异。结论心得安对预防门脉高压症消化道初次出血有明显疗效,但不能延长肝硬化病人的生存期。     

脾动脉结扎联合肝癌切除术治疗肝癌并门静脉高压症临床研究

目的:探讨脾动脉结扎联合肝癌切除术对肝癌并门静脉高压症的治疗效果和临床应用的价值。方法:对2008年10月至2013年10月期间我院收治的84例肝癌并门静脉高压症患者的资料进行回顾性分析,其中脾动脉结扎联合肝癌切除手术的患者50例为研究组,患者34例行肝癌切除及脾切断流术为对照组。比较两组治疗效果及患者术前、术后情况。结果:研究组术前白细胞计数、血小板计数、红细胞计数为(3.1±0.9)×109/L、(58.6±12.7)×109/L、(3.4±0.4)×109/L,术后2周白细胞计数、血小板计数、红细胞计数分别为(5.9±1.5)×109/L、(140.3±50.1)×109/L、(3.6±0.7)×109/L;对照组为术前白细胞计数、血小板计数、红细胞计数为(2.8±1.2)×109/L、(45.8±20.5)×109/L、(3.4±0.4)×109/L,术后2周白细胞计数、血小板计数、红细胞计数为(6.2±0.7)×109/L、(172.5±32.7)×109/L、(3.6±0.3)×109/L。研究组与对照组相比,术后2周白细胞计数、红细胞计数相比差异无统计学意义(P0.05),但术后2周血小板计数研究组低于对照组,差异有统计学意义(P0.05)。研究组术前与术后的白细胞计数、血小板计数、红细胞计数相比,差异均有统计学意义(P0.05)。研究组有17例患者出现术后并发症,占16.0%;对照组有20例患者出现术后并发症,占38.2%;两组对比差异有统计学意义(P0.05)。结论:根据病情合理选择使用脾动脉结扎联合肝癌切除术治疗肝癌并门静脉高压症,可以有效治疗肝癌和脾功能亢进,促进肝功能恢复,对延长原发性肝癌合并肝硬化脾功能亢进患者的生存时间,提高生活质量,具有重要意义。     

Insulin resistance in patients with cirrhosis and portal hypertension

Insulin resistance (IR) is involved in the pathogenesis of endothelial dysfunction and is also present in patients with cirrhosis. Intrahepatic endothelial dysfunction plays a major role, increasing hepatic vascular resistance and promoting portal hypertension (PH). In addition, β-adrenergic agonists and insulin share several intracellular signaling pathways. Thus IR may influence the response to β-blockers. This study aimed at evaluating the relationship between IR and hepatic hemodynamics in patients with cirrhosis and with the portal pressure response to acute β-blockade. Forty-nine patients with cirrhosis and PH were included. Hepatic and systemic hemodynamics were measured, and IR was estimated by using the updated homeostasis model assessment (HOMA)-2 index. Patients with HOMA-2 > 2.4 were considered IR. In patients with hepatic venous pressure gradient (HVPG) ≥ 10 mmHg) [clinically significant PH (CSPH)], hemodynamic measurements were performed again 20 min after intravenous propranolol. Mean HOMA-2 index was 3 ± 1.4. Fifty-seven percent of patients had IR. A weak correlation between HOMA-2 index and HVPG was observed. Eighty-six percent of patients had CSPH. HOMA-2 index was an independent predictor of CSPH. However, in patients with CSPH, the correlation between HOMA-2 index and HVPG was lost. HVPG, but not IR, predicted the presence of esophageal varices. Response to propranolol was not different between patients with or without IR. In nondiabetic patients with cirrhosis, HOMA-2 index is directly associated with the presence of CSPH and indirectly with varices, but does not allow either grading HVPG or predicting its response to propranolol.     

Eicosanoids in cirrhosis and portal hypertension

In the last decade, the knowledge of the pathogenesis of portal hypertension and cirrhosis has increased dramatically. In portal hypertension, almost all the known vasoactive systems/substances are activated or increased and the most recent studies have stressed the importance of the endothelial factors, in particular, prostaglandins. Prostaglandins are formed following the oxygenation of arachidonic acid by the cyclooxygenase (Cox) pathway. An important consideration in portal hypertension and cirrhosis in the periphery is the altered hemodynamic profile and its contributory role in controlling endothelial release of these vasoactive substances. Prostaglandins are released from the endothelium in response to both humoral and mechanical stimuli and can profoundly affect both intrahepatic and peripheral vascular resistance. Within the liver, intrahepatic resistance is altered due to a diminution in sinusoidal responsiveness to vasodilators and an increase in prostanoid vasoconstrictor responsiveness. This review will examine the contributory role of both hormonal and/or hemodynamic force-induced changes in prostaglandin production and signaling in cirrhosis and portal hypertension and the consequence of these changes on the structural and functional response of both the vasculature and the liver.     

Normal fibronectin levels after surgical treatment of portal hypertension in liver cirrhosis.

We found a significantly higher plasma fibronectin concentration in a group of nine cirrhotic patients who underwent surgical treatment for portal hypertension (either shunting and non shunting procedures) when compared to twenty non operated patients. Significantly shorter prothrombin time and activated partial thromboplastin time in the operated patients were found as well. These results might be related to an increased breakdown of fibronectin during consumption coagulopathy taking place in the extended collaterals and reversed in part by surgical treatment of portal hypertension complicating liver cirrhosis.     

Increased plasma volume in two models of portal hypertension in the rat: cirrhosis of the liver and partial portal vein ligation

Portal hypertension has been studied in the rat to see if it is associated to altered blood volume composition, as it has been shown in other species. Plasma volume was measured by isotope dilution using 99mTc labelled albumin in three groups of male Sprague-Dawley rats: normal rats (controls), partially ligated portal vein rats and rats with Cl4C induced cirrhosis. Plasma volume was significantly higher in rats with portal hypertension due to partially ligated portal vein and cirrhosis than in control animals. Similarly, the calculated blood volume was also significantly higher in the portal hypertensive animals than in control group. Portal hypertension in the rat, therefore, has been demonstrated to be associated to a marked hypervolemia and this finding should be taken into consideration in haemodynamic and pharmacokinetic studies in portal hypertensive rat models.     

Alcohol-induced liver cirrhosis as a cause of portal hypertension

Basic data on pathomorphology and symptomatology of the alcohol-induced liver cirrhosis accompanied by portal hypertension are discussed. Respective data were compared with the group of cirrhotic patients not abusing alcohol. A high percentage of encephalopathic disorders and nearly 50% of the patients suffering from the hemorrhage from esophageal varices were the first sign of the cirrhosis in both groups. Despite hemorrhage from esophageal varices a few patients obtained surgical help preventing recurrence of the hemorrhage. Liver functional reserve, incidence of encephalopathies and the degree of liver involvement are in favour for non-alcohol cirrhosis. Inflammatory process in the liver, splenomegaly and hypersplenism were more frequent in the liver cirrhosis of non-alcohol origin.