不同静脉灌注量对门静脉高压失血性休克犬血流动力学的影响

目的 研究门静脉高压犬失血性休克时不同静脉灌注量对血流动力学的影响。方法 行缩窄门静脉主干1/2加丝线慢性栓塞术建立犬肝前性门静脉高压症模型,2周后股动脉快速放血制失血性休克模型,分大剂量、小剂量组静脉灌注复苏休克,观察不同静脉灌注量对门静脉高压失血性休克犬血流动力学的影响。结果 肝前性门静脉高压犬在失血性休克期血流动力学发生一系列改变,加重门静脉高压症时存在的血流动力学紊乱。快速静脉灌注复苏休克后,平均动脉压（MAP）、下腔静脉压（IVCP）、门静脉压（PVP）、门静脉压力梯度（PVPG）、门静脉血流量（PVBF）、肝动脉血流量（HABF）及肝血流量（HBF）均迅速上升,大剂量静脉灌注组升高幅度均较小剂量静脉灌注组大。PVR、SVR、HAR均显著降低。大剂量静脉灌注复苏休克,PVP、PVPG、PVBF、HABF、HBF出现反跳式升高,超过基线水平PVA达（3.28±0.34）kPa。而小剂量静脉灌注复苏休克时PVPG、PVP、PVBF、HABF、HBF与MAP、IVCP改变大致平行,无此反跳式升高,PVP至（2.34±0.26）kPa。大剂量静脉灌往组PVPG较PVP升高更早,更显著,并且超过基础值的 13％,达（2.58±0.37）kPa,故其发生再出血的危险性大为增加。小剂量静脉灌柱组PVPG一直低于基线水平,而且较基础值降低22％以上,至（1.67±0.27）     

硫化氢供体对实验性门静脉高压及内源性一氧化氮/一氧化氮合酶体系的影响

目的探讨硫化氢供体一硫氢化钠（sodium hydrosulfide，NaHS）对大鼠门静脉高压及内源性一氧化氮（nitric monoxide，NO）／一氧化氮合酶（nitricoxide synthase，NOS）体系的影响。方法将30只健康成年雄性sD大鼠随机分为4组：部分门静脉结扎（partly portal vein ligation，PPVL）组（10只）、PPVL＋NariS组（10只）、假手术组（5只）和正常组（5只）。PPVL组和PPVL＋NaHS组行部分门静脉结扎术建立门静脉高压的动物模型。模型制作14天后，分别测定各组大鼠的门静脉压力（PVP）和平均动脉压力（MAP）；采用免疫组织化学检测大鼠肝细胞中一氧化氮合酶（NOS2、NOSS）的蛋白水平表达情况，RT-PCR方法检测大鼠肝组织中NOS2和NOS3的mRNA水平的表达情况。结果术后14d，假手术组和正常组比较，各项检测指标无显著差异，NOS2蛋白及mR-NA水平未见明显表达；NOS3蛋白及mRNA表达水平无显著差异。PPVL组与假手术组比较，PVP明显升高（P〈0．05），MAP则下降（P〈0．05），PPVL＋NaHS组与PPVL组相比较，PVP进一步升高（P〈0．05），MAP则进一步降低（P〈0．05）。PPVL组和PPVL＋NaHS组NOS2在蛋白及mRNA水平均有表达，且后者NOS2蛋白及mRNA表达水平减少（P〈0．05）。4组之间NOS3的蛋白及mRNA表达水平则无显著差异。结论H2S参与了门静脉高压的形成与发展，NaHS可以加重门静脉高压，其作用可能与NO／NOS2体系有关。．     

西地那非与前列腺素E1治疗猪肺动脉高压

目的 比较西地那非和前列腺素E1对幼猪肺动脉高压模型的影响。方法 体质量约5kg实验用健康幼猪24只，用经气管内吸入胎粪法诱发幼猪产生肺动脉高压，2h后建立急性缺氧性肺动脉高压模型。随机将幼猪分成4组：对照组，不给予任何药物治疗;西地那非组，静脉注射枸橼酸西地那非（2mg/kg）、前列腺素E1组，持续静脉滴注前列腺素E120ng/（kg·min）至实验结束;合用组同时给予西地那非组和前列腺素E1。结果 吸入胎粪2h后，记录动物的肺动脉压、肺血管阻力（pulmonary vascular resistance，PVR）和体循环血管阻力（systemic vascular resistance，SVR）。发现肺动脉压、PVR和PVR/SVR均随时间明显增加。施加药物干预以后，西地那非组与合用组的上述指标均明显迅速下降，并且心输出量和心脏指数明显提高;前列腺素E1组肺动脉压、PVR以及PVR/SVR下降程度不如西地那非组明显，心输出量、心脏指数无改善;对照组的肺动脉压、PVR以及PVR/SVR无下降。结论 西地那非降低肺动脉压和肺血管阻力，改善心功能，同时对体循环血流动力学无不良影响;在本实验用量，西地那非扩张肺血管和降低肺血管阻力的作用比前列腺素E1强;两者联合应用没有发生协同降低肺动脉压作用。     

硫化氢对大鼠实验性肝硬化门静脉压力的影响

目的应用内源性硫化氢（H2S）供体硫氢化钠（NaHS）探讨内源性H2S/胱硫醚-γ-裂解酶（CSE）体系对大鼠肝硬化门静脉压力的影响。方法将32只健康雌性SD大鼠随机分为4组：C组和C＋S组采用复合因素法复制肝硬化模型。模型制备52 d后,N＋S组和C＋S组大鼠腹腔注射NaHS 56μmol/（kg.d）,N组和C组腹腔注射同等剂量的生理盐水。1周后分别测定各组大鼠门静脉压力（PVP）及门静脉血浆中H2S含量;采用免疫组织化学方法检测大鼠肝门区门静脉平滑肌细胞中CSE蛋白表达。结果与N组和N＋S组相比,C组和C＋S组PVP均升高,H2S含量及CSE蛋白表达均降低;与C组相比,C＋S组PVP降低,H2S含量及CSE蛋白表达均升高。结论 NaHS作为H2S供体可能具有改善肝硬化大鼠门脉高压的作用,其机制可能与H2S含量及CSE蛋白表达升高有关。     

硝苯吡啶对肝硬化门脉高压病人肝脏血流动力学的影响

硝苯吡啶对肝硬化门脉高压病人肝脏血流动力学的影响许君望，段仲璧，刘宪玲钙通道阻滞剂可降低肝硬化门脉阻力，从而降低门脉压力，但其对肝脏血流动力学的影响尚不清楚。我们采用核多功能仪首次通过法观察了硝苯吡啶（ＮＦＰ）对肝硬化门脉高压病人肝动脉、门静脉血流的...     

门脉高压大鼠门静脉及周围血NO水平观察

目的了解门脉高压鼠血清一氧化氮（ＮＯ）含量变化及意义．方法以部分门静脉结扎大鼠为模型（ｎ＝１２），在部分门静脉结扎及假手术组大鼠（ｎ＝８）术后２周取门静脉血和周围静脉血，采用荧光分析法测量ＮＯ－２含量反应ＮＯ水平．结果门脉高压组门静脉血ＮＯ－２为０７６６μｍｏｌ／Ｌ±００９７μｍｏｌ／Ｌ，周围静脉血为０６８７μｍｏｌ／Ｌ±００９２μｍｏｌ／Ｌ，两者比较相差显著（Ｐ＜００１）；对照组门脉血ＮＯ－２为０６１３μｍｏｌ／Ｌ±００８４μｍｏｌ／Ｌ，周围血为０５９１μｍｏｌ／Ｌ±００４５μｍｏｌ／Ｌ，二者无明显区别（Ｐ＞００５）．门脉高压组与对照组比较，门脉血和外周血中ＮＯ－２含量均显著高于对照组（Ｐ＜００１）．结论门脉高压大鼠血清ＮＯ－２浓度升高，尤以门静脉血含量升高显著，表明门脉高压大鼠血中ＮＯ生成增多，可能在门脉高压症发病中具有一定作用．     

狗肝硬化门脉高压症血浆儿茶酚胺浓度变化的实验研究

本研究通过结扎狗胆总管形成肝硬化门脉高压症的动物模型，对模型成前后门静脉压力、肝静脉压力、门静脉血流量、肝动脉血流量、门静脉血管阻力，肝动脉血管阻力和门静脉、肝静脉、脉主动脉。下腔静脉四部位血浆儿茶酚胺浓度的变化进行了自身对照性对比研究。结果：①肝硬化形成后门脉压力明显增高，肝静脉嵌塞压也明显增高，门脉血流量减少而肝动脉血流量增加，门脉血管阻力增加而肝动脉血管阻力则下降，这些变化与人类肝硬化门脉高压症相同。②门静脉、肝静脉。腹主动脉和下腔静脉血浆去甲肾上腺素的含量均在门脉高压形成后明显增加。提示肝硬化时血浆去甲肾上腺素的增加可能参与门脉高压症的某些病理生理过程，并进一步支持用a受体阻滞剂降低门脉压力和门脉血管阻力，治疗肝硬化食道静脉曲张破裂出血或预防出血。     

不同给药途径对合并肺动脉高压行OPCABG患者血流动力学的影响

目的 评价不同给药途径对合并肺动脉高压行非体外循环冠脉搭桥术（OPCABG）患者血流动力学的影响.方法 择期行OPCABG合并肺动脉高压的冠心病患者30例,随机分为中心静脉输注组（对照组）和肺动脉输注组（观察组）各15例.所有患者麻醉诱导后行右锁骨下静脉穿刺,放置三腔7F中心静脉导管用于输液;右颈内静脉穿刺置入Swan-Ganz导管用于监测血流动力学指标.切皮后对照组和观察组分别通过中心静脉和肺动脉导管给予前列腺素E1.分别于给药前5 min（T0）、给药后3 min（T1）、10 min（T2）、30 min（T3）、60 min（T4）和术毕（T5）记录两组心率（HR）、平均动脉压（MAP）、中心静脉压（CVP）、肺动脉收缩压（PASP）.肺毛细血管楔压（PCWP）和心脏指数（CI）,计算肺血管阻力（PVR）和周围血管阻力（SVR）.结果 两组T1-5时PASP和PVR值均较To明显下降（P均＜0.05）;观察组T1、T2和T5时PASP低于对照组,T1、T2、T3和T5时PVR低于对照组（P均＜0.05）;对照组给药后MAP逐渐下降,SVR也逐渐下降,T1-5时,均低于观察组（P均＜0.05）.T5时,对照组HR明显高于观察组（P＜0.05）.结论 对合并肺动脉高压的冠心病患者行OPCABG时,通过肺动脉输注前列腺素E1可降低肺动脉压同时又不显著影响体循环压力,效果优于经中心静脉输注.     

老年门静脉高压症PCDV手术前后KICG研究

目的进一步提高老年肝硬化门静脉高压症的手术治疗效果。方法采用吲哚氰绿血浆清除率（简称ＫＩＣＧ）为指标，研究了老年肝硬化、门静脉高压症患者在进行ＰＣＤＶ手术前、后ＫＩＣＧ的变化，并与同类中年患者进行比较分析。结果老年肝硬化、门静脉高压症患者ＰＣＤＶ手术前、后ＫＩＣＧ无显著差异（Ｐ＞０．０５），且均低于中年同类患者（Ｐ＜０．０５）。结论（１）ＰＣＤＶ手术对老年肝硬化门静脉高压症患者的肝脏机能和肝脏储备能力影响不大，可做为首选术式。（２）ＫＩＣＧ可做为老年肝硬化门静脉高压症患者手术前确切了解肝脏机能状态和肝脏实际储备能力的可靠指标。（３）ＫＩＣＧ可做为老年肝硬化门脉高压症患者手术前选择手术适应症的指标。（４）ＫＩＣＧ可做为老年肝硬化门脉高压症患者判定手术预后，指导临床治疗的可靠指标。     

吸入依洛前列环素对先天性心脏病继发肺动脉高压患者的急性血管扩张试验

目的探讨吸入依洛前列环素（iloprost）对先天性心脏病（CHD）继发肺动脉高压（PAH）患者的肺动脉压力（PAP）、肺血管阻力（PVR）、心指数（CI）的影响。方法给予34例CHD继发PAH患者吸入iloprost和生理盐水,分别测量吸入iloprost和生理盐水后肺动脉收缩压（SPAP）、肺动脉舒张压（DPAP）、肺动脉平均压（MPAP）、PVR,CI、体循环平均压（MAP）和心率（HR）,比较两组指标的差异。结果吸入iloprost后PAH患者的SPAP、DPAP、MPAP和PVR下降,CI增加,MAP、HR无明显变化。结论吸入iloprost可安全有效地降低PAH患者的PAP和PVR,增加CI。     

Extrahepatic aneurysm of the portal venous system and portal hypertension

Portal venous aneurysm (PVA) is a rare condition characterized by dilatation of the portal venous system. PVA manifestation of symptoms is varied and depends on the aneurysm size, location and related-complications, such as thrombosis. While the majority of reported cases of PVA are attributed to portal hypertension, very little is known about the condition’s pathophysiology and clinical management remains a challenge. Here, we describe a 67-year-old woman who presented with complaint of dyspepsia and without a significant medical history, for whom PVA was incidentally diagnosed. The initial upper abdominal ultrasound revealed marked dilatation of the main portal vein, and subsequent contrast-enhanced computed tomography with angiography revealed a large aneurysm arising from the extrahepatic troncus portion of the portal vein, as well as gastroesophageal varices. A conservative approach using beta-blocker therapy was chosen. The patient was followed-up for 60 mo, during which time the asymptomatic status was unaltered and the PVA remained stable.     

Ultrastructure of the liver in non-cirrhotic portal fibrosis with portal hypertension

The aetiology of the ultrastructural abnormalities of non-cirrhotic portal fibrosis is not known. In an attempt to elucidate the pathophysiology of this condition, the hepatic ultrastructure in nine cases of non-cirrhotic portal fibrosis with portal hypertension has been studied.     

Pathomorphologic study on the extrahepatic portal vein in idiopathic portal hypertension

Patients with idiopathic portal hypertension (IPH) are known to have sclerotic changes of the intrahepatic portal vein radicles. In order to elucidate the pathological changes in the extrahepatic portal venous system in IPH, studies were carried out on the portal trunk in 12 patients with IPH, 59 patients with liver cirrhosis including some with associated hepatocellular carcinoma, and 12 normal matched control subjects. Histological examinations including histomorphometry were performed on the transverse sections of the portal trunk taken at autopsy. Most of the patients with IPH showed severe phlebosclerosis which was more pronounced than seen in liver cirrhosis. Thrombosis was also frequently observed in IPH. In IPH, the portal trunk was characterized by fibrous thickening of the intima and media with a prominent increase of elastic fibers. The mean area and thickness of the intima and media were significantly greater than in patients with liver cirrhosis. Sclerosis extensively involving both the extrahepatic and intrahepatic ramifications of the portal vein appeared to be characteristic of IPH.     

A surgical solution to extrahepatic portal thrombosis and portal cavernoma: the splanchnic–intrahepatic portal bypass

Three cases of prehepatic portal vein thrombosis, complicated by the clinical manifestations of portal hypertension, were successfully treated by surgically created splanchnic–intrahepatic portal bypass. Two out of three patients had been previously submitted to liver transplantation. No significant morbidity was observed and long-term Doppler evaluations proved the patency of the venous grafts.

Together with the technical aspects of the procedures, the possible role of this technique, primarily proposed by De Ville de Goyet in 1992, is discussed in relation to the available therapies for the extrahepatic portal vein thrombosis.     

Non-cirrhotic portal hypertension versus idiopathic portal hypertension

Portal hypertension occurs in a number of disorders other than cirrhosis and they are collectively called non-cirrhotic portal hypertension (NCPH). The common causes of NCPH include idiopathic portal hypertension (IPH), non-cirrhotic portal fibrosis (NCPF) and extrahepatic portal venous thrombosis (EHPVT). Other causes include schistosomiasis, hepatic venous outflow tract obstruction, veno-occlusive disease and congenital hepatic fibrosis. Patients with IPH and EHPVT present with upper gastrointestinal bleeding, splenomegaly, ascites after gastrointestinal bleeding, features of hypersplenism, growth retardation and jaundice due to portal biliopathy. The diagnosis is usually made by abdominal ultrasound, upper gastrointestinal endoscopy, normal liver function tests and normal liver histology. Variceal bleeding in NCPH has lower mortality as compared with cirrhosis because of better liver functions in NCPH. Treatment for NCPH includes primary prophylaxis for variceal bleeding and prevention of repeat bleeding using drugs like beta-blockers, endoscopic sclerotherapy and endoscopic band ligation of varices. In patients with uncontrolled variceal bleeding or symptomatic hypersplenism, porto-systemic shunt surgery or splenectomy are required.