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Ultrastructural changes in cirrhotic and noncirrhotic patients due to hepatectomy
Author(s) -
Wilasrusmee Chumpon,
Siritheptawee Somsak,
Kanchanapanjapon Siroj,
Sopon Prasert,
Vanicha Chaithip,
Limpthong Wichai,
Pongchailerks Paisal,
Lertsithichai Panuwat,
Wilasrusmee Skuntala,
Kittur Dilip S.
Publication year - 2004
Publication title -
journal of hepato‐biliary‐pancreatic surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.63
H-Index - 60
eISSN - 1868-6982
pISSN - 0944-1166
DOI - 10.1007/s00534-004-0902-y
Subject(s) - medicine , pathology , hepatectomy , cirrhosis , bone canaliculus , endoplasmic reticulum , liver biopsy , biopsy , surgery , biology , microbiology and biotechnology , resection
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.