门静脉营养对肝硬化、门静脉高压的影响

目的 探讨门静脉营养在治疗肝硬化、门脉高压症中的作用。方法 将80例入组患者随机分为两组,对照组40,仅予以常规周围静脉肝营养液输入;研究组40,于术后第1d给予肝营养液门静脉内缓慢输入。两组于术后1、2、4w分别检查血清谷丙转氨酶、胆红素及白蛋白,研究组于术中、术后检测自由门静脉压(FPP)。结果 术后1、2、4w血清谷丙转氨酶、血清胆红素下降速度及血清白蛋白升高速度均较对照组快,4w末肝功复常率两组比较差异存在显著性(P<0.05)。研究组术后早期FPP升高,术后随着肝功恢复及侧支循环的建立,FPP逐渐回落。结论 门静脉营养在肝硬化、门脉高压症治疗中,能短时间内较快恢复肝功。肝营养液门静脉内缓慢输入法具有疗效可靠,操作安全等特点。     

Application of ultrasound for the diagnosis of cirrhosis/portal hypertension

Journal of Medical Ultrasonics - With advances in technologic approaches in patients with cirrhosis, including the improvement of management, a simple, one-step approach for advanced fibrotic state...     

多层螺旋CT门静脉造影诊断肝硬化门静脉高压

目的评价门静脉CT血管造影对肝硬化门脉高压患者的诊断价值.方法对43例经临床、肝功能和影像学检查诊断的肝硬化门脉高压患者进行门静脉CT血管成像(CTPV),对门静脉主干、主要属支和侧支循环血管进行显示和测量.结果 43例患者均成功地实施了门静脉CTPV,门静脉主干显示率100%,胃左静脉97.6%,胃短静脉44.2%,食管胃底静脉曲张90.7%,脾/胃肾分流28.7%,脐静脉、腹壁静脉曲张分别为46.5%、44.4%.其中门静脉主干宽度为(13.94±2.47) mm,胃左静脉主干宽度为(5.62±2.40) mm.结论 CTPV可显示肝硬化门脉高压患者的门-体静脉之间侧支循环血管,有助于对门脉高压合并消化道出血患者选择合理治疗方案及进行疗效随访.     

双介入术治疗肝硬化门静脉高压症的临床疗效观察

目的 探讨双介入术治疗肝硬化门静脉高压性上消化道出血、脾功能亢进的临床应用价值及并发症的预防.方法 对32 例确诊为肝硬化门静脉高压合并上消化道出血、脾功能亢进的患者,在超声引导下经皮肝门脉穿刺成功后,将导管超选择插入胃冠状静脉,再经股动脉穿刺插管、超选插入脾动脉分支,混合应用真丝线段、无水乙醇、明胶海绵、不锈钢弹簧圈进行双介入栓塞（胃底-食管曲张静脉及部分脾脏栓塞）治疗.结果 本组32 例PTVE 穿刺成功率为100%,一针穿刺成功率为66%,栓塞成功率100%;PSE 栓塞面积控制在40%～70%;术后24 h～1 周白细胞、血小板明显升高;术后1 个月、6 个月、1 年、2 年和3 年累计再出血率分别为0%、3.1%、12.5%、25%和31.3%;复发出血原因分别为曲张静脉再破裂出血26.1%、门静脉高压性胃病56.5%、消化性溃疡17.4%;所有患者均有不同程度的发热、腹痛、恶心及呕吐等栓塞后综合征,经对症治疗后缓解、症状消失,未发生与手术相关的严重并发症.结论 双介入术治疗门脉高压性上消化道出血、脾功能亢进疗效确切,该方法操作相对简单,侵袭性小,尤其适用于肝功能差难以耐受外科分流及断流手术的患者,具有临床推广应用价值.     

Clinico-pathogenetic and pharmacotherapeutic aspects of portal hypertension in liver cirrhosis

The paper is concerned with the pathogenetic mechanisms of the main manifestations of portal hypertension in liver cirrhosis. The current approaches to pharmacotherapy of hemorrhages from the varicose veins of the esophagus and potential prevention of repeated hemorrhages are evaluated. Different variants of diuretic therapy for ascites are discussed.     

The role of interleukin-6 and nitric oxide in pathogenesis of portal hypertension and decompensation of liver cirrhosis

The study included 49 patients (29 men and 20 women) aged 23-65 years with liver cirrhosis (LC) and 12 (7 men and 5 women) with chronic hepatitis (CH). Etiological factors of LC were hepatitis B and C viruses (in 22 and 16 patients respectively) and alcohol (n=11). Patients with LC showed high levels of blood nitrates and their impaired urinary excretion. In patients with class A LC, nitric oxide levels tended to increase while in those with class B and C LC they were significantly higher than normal. Correlaion analysis revealed the strong dependence of blood nitric oxide level on portal blood flow, hepatic congestion index, the presence of ascitis, and the degree of varicose dilation of oesophageal veins. It also correlated with the serum IL-6 level that increased with deterioration of hepatic function. Patients with class C LC had high IL-6 levels than those with class A and B LC.     

Drug therapy of pulmonary and portal hypertension in liver cirrhosis

Detailed examination of hemodynamics in patients with portal and pulmonary hypertension was performed upon acute drug tests and course administration of nitrosorbide++, corinfar and propranolol. Ultrasound and rheography investigations were employed to elucidate the relations between portal and pulmonary hypertension in cirrhosis patients. Criteria of early diagnosis are discussed. Nitrosorbide++ produced positive effect on hepatic blood flow, corinfar improved pulmonary hemodynamics in lack of its influence on hepatic blood flow, while propranolol resulted in the drop of both portal and pulmonary hypertension, normalization of general hemodynamics.     

彩色多普勒超声对门脉高压食管静脉曲张出血的诊断价值

目的评价门脉血流动力学参数在预测肝硬化食管静脉曲张高危患者中的作用。方法对85例肝硬化患者行胃镜和彩色多普勒超声检查,使用单因素分析和多元分析对门脉血流动力学指标与确认的食管静脉曲张的存在和规模间的关系进行评估。结果食管静脉曲张组的肝动脉阻力指数、脾动脉阻力指数、充血指数、门脉高压指数较无食管静脉曲张组大,肝血管指数较无食管静脉曲张组小,食管静脉曲张重度组的肝动脉阻力指数、脾动脉阻力指数、脾脏长径、充血指数、门脉高压指数较轻-中度组大,肝血管指数较轻-中度组小,差异均有统计学意义（P〈0．05）。结论彩色多普勒超声对门脉高压食管静脉曲张出血有较高的诊断价值。     

常规超声、超声造影以及SWE在肝硬化门静脉高压症TIPS治疗后疗效评价中的应用研究

【】:肝硬化门静脉高压症的发病率逐年升高,经颈静脉肝内门体分流术     

肝硬化食管静脉曲张内镜下皮圈结扎术对门静脉高压性胃病的影响及研究

目的: 分析肝硬化食管静脉曲张内镜下皮圈结扎术（endoscopic varix ligation,EVL）对门静脉高压性胃病（portal hypertensive gastropathy,PHG）的影响。方法: 回顾性分析63例肝硬化PHG患者,其中35例食管静脉曲张行EVL术治疗者为治疗组,28例未行内镜下治疗者为对照组。8周后复查胃镜,观察患者有无PHG加重改变。结果: EVL治疗组中发生PHG加重变者占74.28%（26/35）,对照组中发生PHG加重变者占10.71%（3/28）。经χ²检验,两者间差异有统计学意义(P<0.01)。结论: 食管静脉曲张的EVL治疗可能是PHG发生和加重的重要危险因素。     

Technique innovation of endoscopic ultrasound portal pressure gradient measurement using standard manometer set for portal hypertension assessment

Portal hypertension (PH) is still a major challenge to be managed in clinical practice. However, hepatic vein pressure gradient (HVPG) measurement is not always reliable for portal hypertension (PH) diagnosis. This study showed the impact of endoscopic ultrasound (EUS) as a promising tool for diagnosis and management PH condition.     

肝动脉搏动指数在肝硬化门静脉高压中的应用价值

目的 探讨肝动脉搏动指数(HA-PI)在肝硬化门静脉高压中的应用价值。方法 对50例肝硬化门静脉高压患者和30例健康患者作肝动脉搏动指数检测。结果 病例组HA-PI为1.47±0.19,健康组为1.08±0.13,病例组HA-PI明显高于健康组(P<0.001)。结论 HA-PI在肝硬化门静脉高压中将有重要临床应用价值。     

内源性硫化氢对实验性肝硬化门静脉高压调节作用

目的:探讨内源性硫化氢在实验性肝硬化门静脉高压中的调节作用。方法:32只雌性SD大鼠随机分为4组:肝硬化组、肝硬化+炔丙基甘氨酸组、正常组和正常+炔丙基甘氨酸组,每组各8只。肝硬化组和肝硬化+炔丙基甘氨酸组大鼠采用四氯化碳复合法制备肝硬化门静脉高压动物模型。肝硬化+炔丙基甘氨酸组及正常+炔丙基甘氨酸组大鼠腹腔内注射炔丙基甘氨酸30 mg/(kg.d),肝硬化组及正常组大鼠每日腹腔内给予等量生理盐水。炔丙基甘氨酸干预1周后,采用门静脉导管法测量各组大鼠门静脉压力,用敏感硫电极法检测大鼠血浆内源性硫化氢含量,用免疫组织化学法检测门静脉胱硫醚-γ-裂解酶表达。结果:炔丙基甘氨酸干预1周后,正常组与正常+炔丙基甘氨酸组门静脉压力比较差异无统计学意义(P0.05),肝硬化组较正常组升高(P0.05),肝硬化+炔丙基甘氨酸组较肝硬化组、正常组均升高(P0.05)。血浆内源性硫化氢含量与门静脉胱硫醚-γ-裂解酶蛋白含量在正常+炔丙基甘氨酸组较正常组降低(P0.05),肝硬化组较正常组降低(P0.05),肝硬化+炔丙基甘氨酸组较肝硬化组及正常组均降低(P0.05)。结论:内源性硫化氢在肝硬化门静脉高压形成过程中发挥保护性调节作用。     

Endothelial dysfunction in cirrhosis and portal hypertension

Portal hypertension (PHT) is a common clinical syndrome associated with chronic liver diseases; it is characterized by a pathological increase in portal pressure. Pharmacotherapy for PHT is aimed at reducing both intrahepatic vascular tone and elevated splanchnic blood flow. Due to the altered hemodynamic profile in PHT, dramatic changes in mechanical forces, both pressure and flow, may play a pivotal role in controlling endothelial and vascular smooth muscle cell signaling, structure, and function in cirrhotics. Nitric oxide, prostacyclin, endothelial-derived contracting factors, and endothelial-derived hyperpolarizing factor are powerful vasoactive substances released from the endothelium in response to both humoral and mechanical stimuli that can profoundly affect both the function and structure of the underlying vascular smooth muscle. This review will examine the contributory role of hormonal- and mechanical force-induced changes in endothelial function and signaling and the consequence of these changes on the structural and functional response of the underlying vascular smooth muscle. It will focus on the pivotal role of hormonal and mechanical force-induced endothelial release of vasoactive substances in dictating the reactivity of the underlying vascular smooth muscle, i.e., whether hyporeactive or hyperreactive, and will examine the extent to which these substances may exert a protective and/or detrimental influence on the structure of the underlying vascular smooth muscle in both a normal hemodynamic environment and following hemodynamic perturbations typical of PHT and cirrhosis. Finally, it will discuss the intracellular processes that regulate the release/expression of these vasoactive substances and that control the transformation of this normally protective cell to one that may promote the development of vasculopathy in PHT.     

Splenic haemodynamics and portal hypertension in patients with liver cirrhosis and spleen enlargement

Summary. The relationships between portal hypertension and spleen enlargement, in patients with liver cirrhosis, are not clearly defined; as well as those between splenic haemodynamics and portal hypertension. In 25 cirrhotics with spleen enlargement and portal hypertension and in seven controls, the following parameters were determined: estimated splenic volume (ESV) from the radiographic view of the spleen, according to Blendis, Williams and Kreel (1969), specific splenic blood-flow (SSBF), total splenic blood-flow (TSBF), porto-hepatic gradient (PHG), specific splenic resistance (SSR) and total splenic resistance (TSR). Moreover, the size and extension of oesophageal varices, at oesophagoscopy, were classified according to Dagradi (1973). PHG, ESV and TSBF were increased in all subjects, SSBF was increased in two cases, SSR was increased in two cases and decreased in two cases, TSR was decreased in all cases and ESV was not correlated to the level of portal hypertension. Neither TSBF nor TSR were found to be correlated to the level of portal hypertension, as estimated by PHG or by oesophageal varices. It is concluded that, in patients with liver cirrhosis and spleen enlargement, splenomegaly is likely to be the consequence of pulp hyperplasia and not of passive congestion, and that increases in splenic blood-flow do not contribute significantly to portal hypertension.