Orrego H, Blendis L M, Crossley I R, Medline A, Macdonald A, Ritchie S, Israel Y
Gastroenterology. 1981 Mar;80(3):546-56.
In 70 alcoholic patients the amount of collagen in the space of Disse was compared, using an electron microscopic graded score, to the height of the intrahepatic pressure. A highly significant correlation was found between the amount of collagen and intrahepatic pressure in the group as a whole (r = 0.84; p < 10(-6)), as well as in subgroups of 30 alcoholic patients with normal livers or steatosis (r = 0.83; p < 10(-6)), 9 patients with alcoholic hepatitis (r = 0.81; p < 0.01), and 31 with cirrhosis (r = 0.86; p < 10(-6)). A nonparametric correlational analysis for the complete group also showed a significant relationship (rho = 0.85; p < 10(-6)) between collagen scores and intrahepatic pressure. In 60 patients hepatocyte surface area was measured in the biopsies. In these, hepatocyte surface area significantly correlated with intrahepatic pressure (r = 0.68; p < 10(-7)). No correlation was found between intrahepatic pressure and fat, alcoholic hyalin, or terminal hepatic vein sclerosis. Only with necrosis (r = 0.38; p < 0.001) and inflammation (r = 0.29; p < 0.05) was there a significant relationship with intrahepatic pressure. Chronic ethanol administration for 4 wk in liquid diets to young Wistar rats produced a 50% hepatomegaly due to an increase in hepatocyte size. Intrahepatic pressure in the rats receiving alcohol (19.3 +/- 2.3 mmHg) was significantly higher than in the controls on sucrose (10.4 +/- 0.9 mmHg) (p < 0.01). A highly significant correlation was found between hepatocyte surface area and intrahepatic pressure (r = 0.70; p < 0.005). There was no increase in collagen in the Disse space in these animals. Therefore, hepatomegaly in the absence of an increase in collagen in the Disse space may result in increased intrahepatic pressure. These studies may indicate a sequence of events: hepatomegaly, portal hypertension, and collagenization in the Disse space, which could occur in alcoholic liver disease.
在70例酒精性肝病患者中,采用电子显微镜分级评分法,将狄氏间隙的胶原含量与肝内压进行比较。在整个研究组中,胶原含量与肝内压之间存在高度显著的相关性(r = 0.84;p < 10⁻⁶),在30例肝脏正常或有脂肪变性的酒精性肝病患者亚组中(r = 0.83;p < 10⁻⁶)、9例酒精性肝炎患者亚组中(r = 0.81;p < 0.01)以及31例肝硬化患者亚组中(r = 0.86;p < 10⁻⁶)也是如此。对整个研究组进行的非参数相关分析也显示,胶原评分与肝内压之间存在显著相关性(rho = 0.85;p < 10⁻⁶)。在60例患者的活检标本中测量了肝细胞表面积。在这些患者中,肝细胞表面积与肝内压显著相关(r = 0.68;p < 10⁻⁷)。未发现肝内压与脂肪、酒精性透明小体或终末肝静脉硬化之间存在相关性。仅坏死(r = 0.38;p < 0.001)和炎症(r = 0.29;p < 0.05)与肝内压存在显著关系。给年轻的Wistar大鼠喂饲液体饮食并持续慢性给予乙醇4周,由于肝细胞体积增大导致肝脏肿大50%。接受酒精的大鼠的肝内压(19.3±2.3 mmHg)显著高于接受蔗糖的对照组(10.4±0.9 mmHg)(p < 0.01)。肝细胞表面积与肝内压之间存在高度显著的相关性(r = 0.70;p < 0.005)。这些动物的狄氏间隙中胶原没有增加。因此,在狄氏间隙胶原不增加的情况下肝脏肿大可能导致肝内压升高。这些研究可能表明了一系列事件:肝脏肿大、门静脉高压以及狄氏间隙胶原化,这可能发生在酒精性肝病中。