Frenzel H, Kremer B, Richter I E, Hücker H
Virchows Arch B Cell Pathol. 1976 Jul 21(1):79-90.
Fine structural alterations of liver sinusoids in young and adult albino rats breathing 6% oxygen in nitrogen at normal atmospheric pressure for periods from 3 to 30 h were described by use of TEM and SEM. After short-term hypoxia the fenestrated areas of endothelial cells were partially destroyed. After long--term hypoxia wide gaps could be visualized in the endothelium, too. In the liver specimens of all hypoxic animals electron lucent membrane bounded blebs arose from the endothelial lining. Cytoplasmic protrusions of hepatocytes bulged into the sinusoidal lumen. In the space of Disse and the sinusoidal lumen bleblike corpuscles and parts of cytoplasmic membrane being discharged from liver cell vacuoles could be observed. The find structure of liver sinusoids in hypoxia was very similar in young and adult albino rats. The findings suggest a discharge of metabolites and cellular components from endothelial cells and hepatocytes in a state of energetic insufficiency by forming cellular blebs and protrusions. It was supposed, that the combined effects of hypoxia and shearing of circulating blood were responsible for the development of holes and gaps in the endothelial lining.
利用透射电子显微镜（TEM）和扫描电子显微镜（SEM）描述了正常大气压下在氮气中呼吸6%氧气3至30小时的幼年和成年白化大鼠肝血窦的超微结构变化。短期缺氧后，内皮细胞的窗孔区域部分被破坏。长期缺氧后，内皮中也可见到较宽的间隙。在所有缺氧动物的肝脏标本中，电子透明膜包被的小泡从内皮衬里产生。肝细胞的细胞质突起向肝血窦腔突出。在狄氏间隙和肝血窦腔内，可以观察到泡状小体和从肝细胞空泡中排出的部分细胞质膜。幼年和成年白化大鼠缺氧时肝血窦的精细结构非常相似。这些发现表明，在能量不足的状态下，内皮细胞和肝细胞通过形成细胞小泡和突起释放代谢产物和细胞成分。据推测，缺氧和循环血液剪切力的联合作用是内皮衬里出现孔洞和间隙的原因。
