Morsiani E, Aleotti A, Ricci D
Department of Surgery, University of Ferrara School of Medicine, Arcispedale Sant'Anna, Italy.
J Anat. 1998 May;192 ( Pt 4)(Pt 4):507-15. doi: 10.1046/j.1469-7580.1998.19240507.x.
Rat liver ultrastructure was investigated after partial hepatectomy (PH), by scanning and transmission electron microscopy. Portal pressure was monitored before and after PH and, after killing performed at 6, 12, 24, 48 h and 10 d, regenerating livers were fixed by portal vein perfusion under haemodynamic conditions identical to those existing in vivo. An early and persistent increase in portal pressure after PH was found (P < 0.01 for normal vs sham-operated controls). Ultrastructural study showed sinusoid dilatation and disappearance of the sieve-plate arrangement of small endothelial pores, thus leaving the parenchymal liver cell surface directly exposed to portal blood. Widening of sinusoids, endothelial fenestrations, intercellular spaces and spaces of Disse, was accompanied by dilatation of bile canaliculi. At 10 d, liver ultrastructure had returned to normal. Our observations suggest that a rise in portal pressure, as a consequence of PH, may be related to the observed ultrastructural changes in the liver.
通过扫描电子显微镜和透射电子显微镜对部分肝切除(PH)后的大鼠肝脏超微结构进行了研究。在PH前后监测门静脉压力,并在6、12、24、48小时和10天时处死大鼠后,在与体内相同的血流动力学条件下通过门静脉灌注固定再生肝脏。发现PH后门静脉压力早期持续升高(正常组与假手术对照组相比,P<0.01)。超微结构研究显示肝血窦扩张,小内皮孔的筛板排列消失,从而使实质肝细胞表面直接暴露于门静脉血。肝血窦增宽、内皮窗孔、细胞间隙和狄氏间隙增宽,同时胆小管扩张。在10天时,肝脏超微结构恢复正常。我们的观察结果表明,PH导致的门静脉压力升高可能与肝脏中观察到的超微结构变化有关。