慢性病毒性肝炎肝窦和 Disse腔病变与肝微循环的关系

DISORDERS OF HEPATIC SINUSOIDS AND DISSE SPACE IN CHRONIC VIRAL HEPATITIS :IT'S RELATIONSHIP WITH HEPATIC MICROCIRCULATION

目的 探讨慢性病毒性肝炎肝窦及Disse腔内病变与肝微循环的关系。方法 采用HE及免疫组化染色(SMA、FN、LN及Ⅳ-C),用光镜观察肝活检组织病理学及上述成份的分布,取分级诊断G1～G4、CAHC各30例,CSH10例。设正常肝5例和LC10例作对照。结果 肝窦及Disse腔病理改变有扩张、塌陷、阻塞及狭窄。肝窦塌陷等病变使有效肝窦密度随分级上升而减少,与此同时也可见众多扩张的肝窦及小静脉随分级上升而增多,在G4及CAHC尤为显著。免疫组化显示SMA分布演变尤具特征性,SMA等四种成分在肝内沉着从G1～G4和CAHC逐级增多、增粗、增浓,填塞肝窦和域Disse腔。在CAHC与LC相似。结论 肝窦塌陷等病变使有效肝窦密度减少;扩张的肝窦及小静脉是肝内“功能性捷径”,其中血流快,绕过了肝实质而进入窦后肝静脉系统;肝窦基底膜形成而毛细血管化,其后果是导致肝细胞供血不足。以上病理变化以及肌成纤维细胞的收缩特性,导致肝微循环障碍,严重影响肝细胞的存活及正常功能。

Objective The aim of this study was to explore the disorders of hepatic sinusoids and Disse space in chronic viral hepatitis and it's relationship to hepatic microcirculation. Methods The histopathology, the expression of smooth muscle actin (SMA), fibronectin (FN), laminin (LN) and collagen type IV(C-IV) in sinusoids and Disse space in 160 liver biopsy specimens from patients with hepatitis B,active cirrhrosis (CAHC), chronic severe hepatitis (CSH), were examined by using routine (HE) and immunohistochemistry techniques, respectively. Five normal and 10 cirrhrosis (LC) specimens served as control. Results The pathological changes of hepatic sinusoids were collapsing, occlusive and narrowing,progressively resulting in the sinusoidal density decrease in grading1(G1)-G4;on the contrary, the expansive sinusoids and venular vascular space progressively increased from G1 -G4; they were both obvious in G4 and CAHC. The changes in SMA distribution were characteristic. The spotty activated Ito cells were proliferating , tranforming, expressing SMA, and stretching down the wall of sinusoids or forming fine bundles in Gl or G2;The other 3 elements, FN, IV-C,LN deposited in sinusoids and Disse space,similar to SMA. The higher the gradings, the more the depositing elements. They mainly deposited in the areas of degeneration、inflammation , necroses and fibrous septa. Conclusions The decrease of effective sinusoidal density, capillarization of sinusoids, or the expansive sinusoids and venules, being the intrahepatic functional shunts, can lead to hepatocyte insufficient blood exchange, although unfunctional proliferating blood vessels are present.The contractivity of Ito cell and myofi-broblast cell may also disturb hepatic microcirculation.