内皮素在阻塞性黄疸早期门静脉高压症中的作用

目的初步探讨阻塞性黄疸早期门静脉高压的机制。方法将大鼠分为胆管结扎组（B）与假手术组（A），分别于术后3、7、14d比较两组的游离门静脉压力（FPP）、血浆和肝组织内皮素（ET）浓度。结果胆总管结扎7d后门静脉压力显著高于对照组；胆总管结扎后各时段ET水平均显著高于对照组；门静脉压力与血浆ET、肝组织ET呈正相关。结论阻塞性黄疸早期即有门静脉压力的升高，它可能是体内ET水平升高致肝窦阻力增加的结果。     

AUGMENTED ENDOGENOUS NITRIC OXIDE PRODUCTION IN PARTIAL PORTAL VEIN-LIGATED RATS

1. Endothelium-derived nitric oxide (NO) is a potent vasodilator. Because the body oxidizes it to nitrate ions, NO₃-, measurement of the serum concentration and the urinary excretion of NO₃- may be an index for endogenous NO. We investigated the role of NO on hyperdynamic circulation in cirrhotic and partial portal vein-ligated rats by measuring NO₃. 2. Liver cirrhosis was induced by administration of thioacetamide. Systemic and splanchnic haemodynamics and splenic-systemic shunting were determined by tracer microspheres. The concentration of NO₃- was measured by using high-performance liquid chromatography with an anion-column. 3. We found that systemic and splanchnic hyperdynamic circulation existed to almost the same extent in cirrhotic and in portal vein-ligated rats as compared to the controls and sham-operated rats, respectively. Splenic-systemic shunting was markedly greater in portal vein-ligated rats than in cirrhotic rats. 4. Serum NO₃- levels and urinary excretion of NO₃- in cirrhotic rats tended to increase as compared to the controls. On the other hand, the levels in portal vein-ligated rats were significantly increased as compared to those of the sham-operated rats, and were significantly and negatively correlated to the splanchnic arterial resistance and total vascular resistance. The amount of urinary excretion of NO₃- significantly correlated to splenic-systemic shunting (r = 0.61, P<0.05) only in portal vein-ligated rats. 5. We suggest that these high levels of NO₃- in portal vein-ligated rats relate to the extensive formation of porto-collateral vasculature or acute changes in systemic and splanchnic haemodynamics due to portal vein-ligation.     

Transjugular intrahepatic cavoportal shunt for Budd–Chiari syndrome

Budd–Chiari syndrome (BCS) is characterized by obstruction of the hepatic venous outflow tract. Therapeutic options for BCS are limited. We report a case of a 21-year-old woman with protein S and C deficiency with gross ascites. Treatment with transjugular intrahepatic portosystemic shunt (TIPS) was attempted, which revealed occluded hepatic veins, so transcaval TIPS was performed. No serious procedure-related complication occurred. After successful shunt creation, the patient's symptoms subsided and she was discharged and followed up for 6 months.     

生长抑素治疗食管胃底静脉曲张破裂出血的临床研究

目的 探讨生长抑素治疗食管胃底静脉曲张破裂出血的临床效果。方法 应用奥曲肽治疗食管胃底静脉曲张破裂出血患者41例,并与垂体后叶素治疗的32例及三腔管治疗的25例进行对照。观察3组平均止血时间、24h止血率以及治疗前后门静脉主干直径、血流速度、血流量的变化。结果 奥曲肽治疗组、垂体后叶素治疗组、三腔管治疗组平均止血时间分别为194.27±28.88min、358.11±151.43min、134.71±32.12min,24h止血率分别为63.41％、37.50％、72％。奥曲肽治疗组止血率显著高于垂体后叶素治疗组(P<0.01)。奥曲肽治疗前后门静脉内径分别为10.86±0.41mm、13.84±0.35mm,二者有显著差异。奥曲肽治疗后其门静脉血流速度,血流量与治疗前相比较也有显著差异(P<0.01,P<0.05)。结论 奥曲肽能使门脉内径相对缩小、血流量减少和血流速度加快,从而使门脉压力降低达到止血的目的。     

改良Sugiura术与青木春夫式断流术的比较

目的评价改良Sugiura术的疗效。方法回顾性分析2001年3月～2004年12月施行的改良Sugiura术50例患者的临床资料，并与随机抽取的以往施行的青木春夫式断流术50例做比较。结果改良Sugiura术：术后发生并发症10例，手术死亡5例，远期出血5例，肝性脑病3例，术后死亡4例；青木春夫式断流术：术后发生并发症7例，手术死亡2例，远期出血6例，肝性脑病2例，术后死亡4例，上述指标两者比较差异均无统计学意义，P〉0．05。改良Sugiura术手术时间和住院时间分别为（2．6±0．9）h、（27．5±10．5）d，显著短于青木春夫式断流术的（3．8±0．8）h和（53．2±34．2）d，P〈0．01。结论改良Sugiura术总体疗效肯定，是一种较好的青木春夫式断流术的替代手术，其操作简便，手术时间和住院时间短，值得临床推广。     

肠腔侧侧分流术治疗门静脉高压症的体会

本文报道了肠系膜上静脉与下腔静脉侧侧分流术7例,并介绍了手术的体会,认为应解剖、暴露肠系膜上静脉“外科干”与相应平面的下腔静脉,清除两者间的增生组织,缩短两者的间距,才易取得手术成功。本术既可使门静脉压下降适中,又对门静脉向肝血流干扰较小,且对组织损伤较轻。     

HO-1、HO-1 mRNA在肝硬化病人肝组织中的表达及与门静脉压力的关系

目的　观察HO CO系统在肝硬化病人肝组织中的表达及与门静脉压力的关系 ,以探讨其在肝硬化门脉高压中的作用。方法　随机选取 2 0例正常志愿者及 2 0例肝硬化患者 ,在B超引导下经皮经肝穿刺分别测定门静脉压力、抽取门静脉血和外周血并留取肝组织 ,测定血液中CO浓度 ,用免疫组化和RT PCR方法观察肝组织HO 1及其HO 1mRNA的表达。结果　肝硬化病人下腔静脉及门静脉血中CO浓度、肝组织HO 1、HO 1mRNA的表达及门静脉压力均分别显著高于正常对照组 ,正常对照组的外周血和门静脉血中CO浓度水平接近 ,无明显差异 ;但肝硬化患者的门静脉血CO浓度显著高于外周血CO浓度。结论　门脉血CO浓度、肝组织中HO 1以及HO 1mRNA表达与门静脉压力密切相关     

Changes of hepatic and systemic haemodynamics following somatostatin administration in patients with hepatitis B-related cirrhosis

Abstract Somatostatin has been used to effectively control acute variceal haemorrhage, with conjectured mechanisms on portal hypertension. We, therefore, evaluated the effects of somatostatin on hepatic and systemic haemodynamics in 15 patients with hepatitis B-related cirrhosis and portal hypertension. All patients received an intravenous, continuous infusion of somatostatin 250 μg/h, following a bolus injection of 250 μg. In systemic haemodynamics, the mean arterial pressure (MAP) increased ( P < 0.05), associated with a reflex bradycardia within 3 min following bolus injections, compared with basal values. The right atrial pressure, pulmonary capillary wedge pressure, inferior vena cava pressure, cardiac index, and systemic vascular resistance remained unaffected after drug infusion. In hepatic haemodynamics, the wedge hepatic vein pressure remained unchanged after drug administration. However, there was an increase in free hepatic vein pressure (FHVP; P < 0.05), and a trend toward a decrease in the hepatic vein pressure gradient (HVPG; P = 0.063), within 3 min after bolus injection. Furthermore, the hepatic blood flow decreased significantly at 10 and 30 min after somatostatin infusion ( P < 0.05). The effective sinusoidal perfusion assessed by indocyanine green infusion also decreased progressively at 10 min ( P = 0.057) and 30 min ( P < 0.05). We concluded that somatostatin, at the dose used in this study, caused a transient and bolus-related vasoconstrictive effect, resulting in increases in MAP and FHVP, a decrease in heart rate, and a trend toward lower HVPG. In addition, somatostatin reduced the hepatic blood flow and effective sinusoidal perfusion which may be hazardous to cirrhotic patients during variceal haemorrhage.     

Lactate dehydrogenase activity and isoform distribution in normal and hypertrophic smooth muscle tissue from the rat

The lactate dehydrogenase (LDH) activity and isoform distribution of LDH were investigated in tissue samples from the rat portal vein, aorta and urinary bladder. In addition, samples were obtained from hypertrophic urinary bladder. The total LDH activity per unit smooth muscle volume was higher in the urinary bladder compared to that in portal vein and aorta. Five LDH isoforms, reflecting different combinations of the two polypeptide chains denoted H and M, could be separated by agarose gel electrophoresis. The aorta contained more of the H form compared to the portal vein and urinary bladder. This difference suggests that the aorta, which is a slow smooth muscle, is more adapted for aerobic metabolism than the faster muscles of portal vein and urinary bladder. In the hypertrophic urinary bladder a shift in LDH isoform pattern towards less of the H form was found, which correlates with a better maintenance of contraction in anoxia in this type of hypertrophic smooth muscle.