肝切除术对肝硬化和非肝硬化患者超微结构的影响。

Chumpon Wilasrusmee, Somsak Siritheptawee, Siroj Kanchanapanjapon, Prasert Sopon, Chaithip Vanichanon, Wichai Limpthong, Paisal Pongchailerks, Panuwat Lertsithichai, Skuntala Wilasrusmee, Dilip S Kittur
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引用次数: 12

摘要

背景/目的:在不可逆细胞损伤的早期阶段,超微结构水平的改变可以在组织学改变之前被识别出来。本研究的目的是比较肝硬化和非肝硬化肝脏对肝切除术后缺血和再灌注损伤的超微结构变化。方法:采用相同的技术对肝硬化和非肝硬化患者进行肝切除术。在剖腹手术后立即、肝门钳松解前(缺血期)和再灌注后30-45分钟,对每位患者未切除部分肝脏的3个活检标本(Tru cut)进行透射电镜观察。结果:除1例肝硬化患者死于肝功能衰竭外,所有患者术后均恢复良好。15例患者的手术时间、出血量和流入阻塞次数均无显著差异。我们发现10例非肝硬化患者和4例肝硬化患者的形态学变化相同。缺血期的变化包括核膜畸形、核缘局灶性染色质凝聚、线粒体和内质网肿胀。在再灌注期,部分肝细胞细胞核和线粒体内颗粒发生早期不可逆变化,细胞质空泡化增加。内皮细胞、Kupffer细胞、胆管和Ito细胞在缺血期和再灌注期均未受影响。然而,在1例肝硬化肝衰竭死亡患者中,缺血期线粒体嵴明显肿胀和扩张,再灌注期Ito细胞出现畸形。结论:这是首个关于肝硬化患者肝切除术后超微结构改变的报道,我们发现除了1例肝硬化患者术后肝功能衰竭外,其超微结构变化与非肝硬化患者相同。
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Ultrastructural changes in cirrhotic and noncirrhotic patients due to hepatectomy.

Background/purpose: Alterations at the ultrastructural level can be identified prior to histological change in the early phase of irreversible cell damage. The aim of this investigation was to compare the ultrastructural changes in cirrhotic and noncirrhotic liver in response to ischemic and reperfusion injury due to hepatectomy.

Methods: Hepatic resections using the same technique were performed in cirrhotic and noncirrhotic patients. Three biopsy specimens (Tru cut) from each patient, in the unresected part of the liver, were studied by transmission electron microscopy: immediately after laparotomy, before releasing of the porta hepatis clamp (ischemic phase), and 30-45 min after reperfusion.

Results: All patients did well after surgery, except for 1 cirrhotic patient who died of liver failure. There were no significant differences in operative time, blood loss, and inflow occlusion times in any of the 15 patients. We found that morphological changes were the same in the 10 non-cirrhotic and 4 cirrhotic patients. Changes during the ischemic phase included nuclear membrane deformity, focal chromatin condensation at the nuclear margin, and swelling of both mitochondria and endoplasmic reticulum. In the reperfusion phase, there were early irreversible changes in the nuclei of some hepatocytes and intramitochondrial particles and increased vacuolization in cytoplasm. Endothelial cells, Kupffer cells, bile canaliculi, and Ito cells were not affected in either the ischemic or the reperfusion phase. However, in the 1 cirrhotic patient who died of liver failure, there were marked swelling and dilated cristae in mitochondria during the ischemic phase and deformity of Ito cells during the reperfusion phase.

Conclusions: In this, the first report of ultrastructural changes due to hepatectomy in cirrhotic patients, we found that the changes were the same as those in non-cirrhotic patients, except for the one cirrhotic patient who had postoperative liver failure.

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