肝硬化门静脉高压侧支循环的形成及临床意义

门静脉高压是一种常见的临床疾病,其带来的一系列并发症包括消化道曲张静脉形成、腹水、肝性脑病、腹壁静脉曲张等,这些并发症大多与门静脉压力增高后侧支循环开放有关,一方面这些侧支循环可缓解门静脉部分压力,但另一方面会给患者带来相应的并发症。综述了近年来有关门静脉高压侧支循环的报道与研究进展,以提高对门静脉高压侧支循环的认识,从而提高该类疾病的临床诊治。     

门静脉高压症特殊侧支循环的临床意义及诊治

随着对门静脉高压症病理生理机制的深入认识以及检查手段的丰富和精细,门静脉高压症所致的特殊侧支循环不断被发现和了解。因其临床表现多样、诊断困难、治疗棘手、并发症严重、预后较差、病死率高,对其早期识别和诊断及制订合理有效的治疗方案是临床上需要解决的难题。本文将对门静脉高压症导致的特殊侧支循环从解剖结构、临床意义、诊断方法以及治疗手段等方面进行总结阐述。     

门静脉高压侧支循环与血管内皮细胞生长因子

新近发现门静脉高压侧支循环形成与血管内皮细胞生长因子(VEGF)诱导的血管生成有一定的关系,这对传统认为的门静脉压力增高引起被动的血管通道开放的理论提出了挑战．研究提示在门静脉高压动物中VEGF／VEGF-R2 通路促进了门静脉系统侧支血管和高动力循环的形成．从而证实门静脉高压症侧支循环形成不仅归咎于连接门体静脉系统的分支血管, 而且是VEGF依赖的血管生成结果．现就近来这方面研究的文献作一综述．     

螺旋CT门静脉造影对门脉高压侧支循环的研究

目的探讨多排螺旋CT门静脉造影(CT portal venography,CTPV)显示肝硬化门脉高压侧支循环血管的临床应用价值。方法对92例肝硬化门脉高压的患者分别进行CT门脉造影,获得门脉侧支循环血管的清晰图像,测量门静脉主干和胃左静脉直径,将胃镜与CT门静脉造影两种技术进行比较。结果应用CT门静脉造影能清晰显示和测量门脉侧支循环的血管。CT门静脉造影与胃镜两种方法对食管和胃底曲张静脉的显示能力具有一致性,Kappa值分别为0.502和0.478。结论应用多排螺旋CT门静脉造影能很好显示和测量门体间侧支循环血管。联合应用多排螺旋CT门静脉造影与胃镜两种方法,对于肝硬化门静脉高压患者的诊断、病情判断和估计预后有帮助。     

脾脏在特发性门静脉高压症形成中的作用研究

转发性门静脉高压症（IPH）是病因不明的疾病，本研究的目的是探讨脾大的发生机制及脾脏血流量在IPH形成中的作用。     

多普勒导丝评价猪急性冠状动脉闭塞侧支循环状态及硝酸甘油的影响

目的应用冠状动脉内多普勒导丝评价猪冠状动脉急性闭塞后侧支循环状况及硝酸甘油对其的影响.方法使用冠状动脉内多普勒导丝测定14头小型家猪正常状态及左回旋支急性闭塞后远端血管的血流频谱,并观察冠状动脉内应用硝酸甘油对其的影响.结果急性闭塞左回旋支远端的平均峰值流速(APV)明显低于正常[(0.97±1.05)cm/svs.(25.78±4.36)cm/s,P<0.01];应用硝酸甘油后梗死相关血管(IRA)血流呈现逆向或双向,APV绝对值较用药前明显增加[(0.97±1.05)cm/svs.(8.32±1.53)cm/s,P<0.01];闭塞后90 min基础及重复用药后APV分别为(0.99±1.14)cm/s和(9.02±1.47)cm/s,较闭塞即刻差异均无统计学意义.结论多普勒导丝可用来评价冠状动脉侧支循环,猪急性冠状动脉闭塞时侧支循环自身建立不足,硝酸甘油可明显增加冠状动脉侧支循环血流.     

经颅多普勒评估颈内动脉系统动脉闭塞患者的侧支循环代偿能力

目的 探讨颈内动脉系统动脉闭塞患者的侧支循环代偿能力。方法 对213例颈内动脉系统动脉闭塞患者，采用经颅多普勒技术检测颅内侧支循环通路。结果 颈内动脉颅外段闭塞，经颅多普勒显示眼动脉侧支通路开放58％，前交通动脉侧支通路开放93％，后交通动脉侧支通路开放60％。颈内动脉远段闭塞，经颅多普勒显示眼动脉侧支通路开放15％，前交通动脉侧支通路开放51％，后交通动脉侧支通路开放61％。大脑中动脉主干闭塞患者均出现软脑膜吻合侧支循环，91％病侧大脑前动脉血流速度代偿性增快，9％病侧大脑后动脉血流速度代偿性增快。15例（7％）未发现侧支循环，108例（55％）1个侧支通路建立，79例（40％）2个侧支通路建立，11例（5％）3个侧支通路建立。结论 经颅多普勒有助于了解颈内动脉系统动脉闭塞患者的侧支循环代偿能力，为评价治疗效果和预后提供了重要的客观依据。     

冠状动脉内多普勒超声评价酚妥拉明对猪急性冠状动脉闭塞侧支循环的影响

目的:应用冠状动脉内多普勒超声评价猪急性闭塞冠状动脉侧支循环情况及酚妥拉明对其影响。方法:使用冠状动脉内多普勒超声测定14头小型家猪正常状态及急性闭塞后左回旋支的血流频谱,并观察冠状动脉内应用酚妥拉明对其影响。结果:急性闭塞后回旋支远端的平均峰值流速(APV)明显低于正常(0.97±1.05)∶(25.78±4.36)cm/s,P<0.01);应用酚妥拉明后梗死血管变为反向或双向血流,APV绝对值[(8.54±2.15)cm/s]较用药前明显增加(P<0.01);闭塞90min后肝酚妥拉明APV为(8.95±2.36)cm/s,较闭塞即刻差异有统计学意义(P<0.01)。结论:冠状动脉内多普勒超声可用来评价冠状动脉侧支循环,猪急性冠状动脉闭塞时侧支循环自身建立不足,酚妥拉明可明显增加冠状动脉侧支循环血流。     

彩色多普勒超声诊断区域性门静脉高压症的价值

为早期诊断区域性门静脉高压症,探讨彩色多普勒超声的诊断价值。回顾性分析了经临床证实的11例患者的病史、超声学特征,分析了彩色多普勒超声诊断对于该病的诊断正确率和病因诊断符合率。结果表明,11例经彩色多普勒超声诊断的正确率为100％,病因符合率为90.9％。由于彩色多普勒超声具有简单、无创、准确等优点,应作为区域性门静脉高压症的首选诊断方法。     

Effects of α1 and β-adrenergic antagonists and 5-hydroxytryptamine receptor antagonist on portal-systemic collateral vascular resistance in conscious rats with portal hypertension

In order to study the acute effects of pharmacological agents on the vascular resistance of portal-systemic collaterals, a model of total portal vein occlusion with 100% portal-systemic shunts was developed in the conscious rat. The haemodynamic effects of several vaso-active substances were evaluated in this model and compared with those obtained after saline administration. Prazosin (0.5 mg), an alpha 1-adrenergic antagonist, significantly reduced mean arterial pressure by 29%, portal pressure from 13.8 +/- 1.0(mean +/- s.e.m.) to 10.1 +/- 0.4 mmHg and portal tributary blood flow (radioactive microspheres) from 13.6 +/- 2.1 to 11.7 +/- 1.2 mL/min. It also decreased portal-systemic vascular resistance from 95 +/- 16 to 73 +/- 9 dyn s/cm5 x 10(3). Propranolol (4 mg), a beta-adrenergic antagonist, significantly reduced mean arterial pressure by 12% and portal pressure from 15.5 +/- 1.2 to 13.3 +/- 0.9 mmHg while reducing portal tributary blood flow from 14.6 +/- 1.5 to 11.0 +/- 1.7 mL/min and increasing portal systemic collateral vascular resistance from 88 +/- 7 to 103 +/- 8 dyn s/cm5 x 10(3). Ketanserin (0.25 mg/kg), a 5-hydroxytryptamine receptor antagonist, reduced portal pressure from 15.8 +/- 1.0 to 13.3 +/- 0.7 mmHg at a dose that did not alter mean arterial pressure or portal tributary blood flow. It achieved this by reducing portal-systemic collateral vascular resistance from 90 +/- 14 to 74 +/- 13 dyn s/cm5 x 10(3). Saline had no significant effect on systemic and splanchnic haemodynamics. This study shows that ketanserin decreases vascular resistance of portal-systemic collaterals while propranolol increases it. Thus, it is suggested that collateral vascular resistance is accessible to pharmacological manipulation.     

Successful choledochojejunostomy for choledochal stricture with preservation of the collateral parabiliary venous system following iatrogenic portal occlusion

We surgically treated a patient with biliary stricture and portal vein occlusion, after operation for gastric cancer with lymphadenectomy along the hepatoduodenal ligament, that had led to choledochal stone formation and a dilatated parabiliary venous system. A 57-year-old man without hepatic dysfunction exhibited hepatic duct dilatation with choledochal stone on ultrasonography and percutaneous transhepatic cholangiography, respectively. Pharmacoportography revealed occlusion of the portal vein and dilatation of the parabiliary venous system. Of various preoperative imaging studies used, enhanced computed tomography was most useful for delineating the surgical anatomy of the hepatoduodenal ligament. Complete preservation of the dilatated vessels, which functioned as the main portal collateral pathway, resulted in a successful choledocho-jejunostomy, with an uneventful postoperative course.     

特发性门静脉高压症的彩色多普勒超声诊断与临床价值

目的探讨特发性门静脉高压症（IPH）的声像图特征,评价彩色多普勒对IPH的临床诊断价值。方法对25例IPH患者进行彩色多普勒超声检查,观察肝脏表面、内部回声、脾脏大小及肝内外门静脉系统等。结果25例患者中,25例均见门静脉肝内分支管壁增厚、回声增强、管腔狭窄甚至闭塞,15例实质回声增粗,门静脉海绵样变性22例,门静脉系统血栓5例,均为门静脉主干、脾静脉及肠系膜上静脉血栓,15例伴有胆道系统的异常。结论临床上不明原因的门脉高压及脾功能亢进患者均应进行彩色多普勒超声检查,肝内门静脉分支管壁增厚、管腔狭窄甚至闭塞的特征性改变及门静脉海绵样变性可提示IPH。     

The hypotensive effect of oral nitroglycerin on portal venous pressure in patients with cirrhotic portal hypertension

Abstract Nitroglycerin was administered orally to seven patients with cirrhosis and portal hypertension, to determine whether portal venous pressure (PVP) may be lowered without the systemic effects associated with its intravenous or sublingual use. PVP was measured via direct cannulation of the portal vein transhepatically using a Chiba needle. PVP decreased from 29 (s.d. = 4) to 22.7 (s.d. = 3.7) mmHg (22% mean fall) following 1.2 mg nitroglycerin with onset 7–15 min following ingestion, and the response persisted for up to 150 min. This was not associated with headache in any patient. Although a decrease in blood pressure was seen in most patients, this temporally followed the fall in PVP suggesting that it was a secondary response. Sublingual nitroglycerin was given to two patients without change in PVP yet both experienced severe headache. These findings support the hypothesis that oral nitroglycerin is delivered differentially to the portal venous bed with differential effects on PVP. Further studies are needed to evaluate this agent and this strategy for their potential role in long-term control of portal pressure.     

Endothelial dysfunction in the regulation of cirrhosis and portal hypertension

Portal hypertension is caused by an increased intrahepatic resistance, a major consequence of cirrhosis. Endothelial dysfunction in liver sinusoidal endothelial cells (LSECs) decreases the production of vasodilators, such as nitric oxide, and favours vasoconstriction. This contributes to an increased vascular resistance in the intrahepatic/sinusoidal microcirculation and develops portal hypertension. Portal hypertension, in turn, causes endothelial dysfunction in the extrahepatic, i.e. splanchnic and systemic, circulation. Unlike dysfunction in LSECs, endothelial dysfunction in the splanchnic and systemic circulation causes overproduction of vasodilator molecules, leading to arterial vasodilation. In addition, portal hypertension leads to the formation of portosystemic collateral vessels. Both arterial vasodilation and portosystemic collateral vessel formation exacerbate portal hypertension by increasing the blood flow through the portal vein. Pathological consequences, such as oesophageal varices and ascites, result. While the sequence of pathological vascular events in cirrhosis and portal hypertension has been elucidated, the underlying cellular and molecular mechanisms causing endothelial dysfunctions are not yet fully understood. This review article summarizes the current cellular and molecular studies on endothelial dysfunctions found during the development of cirrhosis and portal hypertension with a focus on the intra‐ and extrahepatic circulations. The article ends by discussing the future directions of the study for endothelial dysfunction.