Frenzel H, Hücker H, Kremer B
Virchows Arch A Pathol Anat Histol. 1977 Aug 9;375(1):37-51. doi: 10.1007/BF00430643.
Changes in liver sinusoids following fractionated irradiation were studied by use of TEM and SEM. Rats received telecobalt-irradiation of their liver regions in daily doses of 500 r for 9 days, a total dose of 4500 r. One day after the end of the irradiation series the fine structure of hepatocytes was almost intact. In SEM the liver sinusoids contained numerous corpuscles, which in TEM were recognized as cellular blebs separated from endothelial cells. 8 days after irradiation small foci of necrotic hepatocytes could be visualized. Instead of complexes of small fenestrations (sieve plates) the endothelial cells contained striking round or oval holes in their tenuous processes. After 120 days small groups of hepatocytes with alterated fine structure of their organelles and some necrotic parenchyma cells were still present. Away from these focal necroses the endothelial cells now resembled sinusoidal endothelium in control animals. Fat-storing cells appeared to have multiplied and were enlarged. There was distinct fibrosis only in perisinusoidal spaces. The formation and discharge of electron lucent blebs is discussed as a mechanism compensating for an enhanced uptake of fluid into irradiation injured endothelial cells. In order to form holes in the tenuos processes of endothelial cells a disordered synthetic pattern and the shearing forces of the circulating blood are thought to be necessary. Repair of these intracellular holes may be possible. In rats irradiation induced lesions of the small intrahepatic vessels can be excluded as a cause of the late changes in liver parenchyma cells.
通过透射电子显微镜（TEM）和扫描电子显微镜（SEM）研究了分次照射后肝血窦的变化。大鼠接受肝脏区域的远距钴照射，每日剂量为500伦琴，共照射9天，总剂量为4500伦琴。照射系列结束后一天，肝细胞的精细结构几乎完好无损。在扫描电子显微镜下，肝血窦内含有大量小体，在透射电子显微镜下这些小体被识别为与内皮细胞分离的细胞泡。照射8天后，可以看到坏死肝细胞的小病灶。内皮细胞的细薄突起中没有小窗孔（筛板）复合体，而是含有明显的圆形或椭圆形孔。120天后，仍存在一小群细胞器精细结构改变的肝细胞和一些坏死的实质细胞。远离这些局灶性坏死区域，内皮细胞现在类似于对照动物的肝血窦内皮。贮脂细胞似乎增殖并增大。仅在肝血窦周围间隙有明显的纤维化。电子透明泡的形成和释放被认为是一种机制，可补偿照射损伤的内皮细胞对液体摄取的增加。为了在内皮细胞的细薄突起中形成孔，紊乱的合成模式和循环血液的剪切力被认为是必要的。这些细胞内孔可能是可以修复的。在大鼠中，可以排除照射引起的肝内小血管病变是肝实质细胞后期变化的原因。
