Shibayama Y, Hashimoto K, Nakata K
Department of Pathology, Osaka Medical College, Takatsuki City, Japan.
J Pathol. 1990 Sep;162(1):77-81. doi: 10.1002/path.1711620114.
Vacuolation of liver cells, which is often seen in patients with right-sided heart failure, is sometimes confused with fatty change, but the contents are components of blood. This study was undertaken using an isolated rat liver perfusion model to clarify the pathogenesis of vacuolation of liver cells. It has been demonstrated that (1) hypoxia alone cannot cause vacuolation; (2) elevation of the sinusoidal pressure leads to vacuoles in liver cells, irrespective of the oxygen content of the perfusate; and (3) the number and size of vacuoles are proportional to the height of the sinusoidal pressure, but not to the oxygen content of the perfusate. The reason why vacuolation generally appears in the pericentral area in patients with right-sided heart failure may be that the sinusoidal pressure in this area rises in parallel with the inferior vena cava pressure.
肝细胞空泡化在右心衰竭患者中较为常见，有时会与脂肪变性相混淆，但空泡内容物为血液成分。本研究采用离体大鼠肝脏灌注模型，以阐明肝细胞空泡化的发病机制。结果表明：（1）单纯缺氧不会导致空泡化；（2）无论灌注液中的氧含量如何，肝血窦压力升高均会导致肝细胞出现空泡；（3）空泡的数量和大小与肝血窦压力的高度成正比，而与灌注液中的氧含量无关。右心衰竭患者的空泡化通常出现在肝小叶中央区的原因可能是该区域的肝血窦压力随下腔静脉压力同步升高。
