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ISRN Surgery  2013 

The Effects of Bile Duct Obstruction on Liver Volume: An Experimental Study

DOI: 10.1155/2013/156347

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Abstract:

Objectives. This study is aimed at investigating alterations in liver volume during obstructive jaundice in rat liver. Materials and Methods. Thirty-six rats were divided into four groups. Abdominal tomography was performed for baseline volumetric analyses. The main bile ducts were ligated (BDL). Volumetric analyses were repeated 3 days after BDL in group 1, 7 days after BDL in group 2, 15 days after BDL in group 3, and 25 days after BDL in group 4, and total hepatectomy was performed in all animals. Control group ( ) was created with the rats that died before bile duct ligation. Results. There was no difference found in liver volume in group 1 compared to control animals. The liver volume was increased 7 days after BDL ( ). It was increased up to 60% of baseline values 25 days after BDL ( ). Wet liver weights of animals were also increased compared to control group. Liver weights were increased up to 40% percent of baseline values in group 4 ( ). Conclusions. Liver volume and weight were increased after BDL. Liver surgery in patients with huge liver mass is generally associated with significant difficulty. The surgeon should be aware of the time-dependent alteration in liver volume after obstructive jaundice. 1. Introduction Chronic cholestatic liver disease and bile duct tumors are the main causes of chronic cholestasis in daily clinical practice. Postcanalicular biliary obstruction leads to bile duct epithelial cell proliferation and periportal fibrosis [1–3]. Clinical and experimental studies have found that only the timely restoration of bile flow can halt fibrosis and reverse biliary hyperplasia [4–6]. The role of bile duct obstruction on liver volume has not been evaluated in detail. Thus, the aim of this study was to identify the time-dependent alterations on liver volume after bile duct ligation. 2. Materials and Methods Thirty-six male Sprague-Dawley rats weighing between 180 and 300?g were used for the study. They were kept under routine laboratory conditions and received standard laboratory chow with free access to food and water. The study protocol was approved by the institutional Ethics Committee for Experimental Studies at February 3, 2010, document number: 01/2010. 2.1. Experimental Design The animals were divided into four groups of 8 animals. Weight measurement and abdominal tomography under intraperitoneal ketamine (50?mg/kg, Ketalar, Parke-Davis, Ann Arbor, Michigan, USA) anesthesia for volumetric analyses were performed before bile duct ligation (BDL). In group 1 ( ), abdominal tomography (CT) was performed 3 days after BDL for

References

[1]  J. S. Morris, G. A. Gallo, P. J. Scheuer, and S. Sherlock, “Percutaneous liver biopsy in patients with large bile duct obstruction,” Gastroenterology, vol. 68, no. 4 I, pp. 750–754, 1975.
[2]  P. A. Slott, M. H. Liu, and N. Tavoloni, “Origin, pattern, and mechanism of bile duct proliferation following biliary obstruction in the rat,” Gastroenterology, vol. 99, no. 2, pp. 466–477, 1990.
[3]  T. F. Tracy Jr., A. J. Tector, M. E. Goerke, S. Kitchen, and D. Lagunoff, “Somatostatin analogue (octreotide) inhibits bile duct epithelial cell proliferation and fibrosis after extrahepatic biliary obstruction,” The American Journal of Pathology, vol. 143, no. 6, pp. 1574–1578, 1993.
[4]  G. A. D. McPherson, I. S. Benjamin, H. J. F. Hodgson, N. B. Bowley, and D. J. Allison, “Pre-operative percutaneous transhepatic biliary drainage: the results of a controlled trial,” British Journal of Surgery, vol. 71, no. 5, pp. 371–375, 1984.
[5]  P. S. Bhathal and J. A. M. Gall, “Origin and involution of hyperplastic bile ductules following total biliary obstruction,” Liver, vol. 10, no. 2, pp. 106–115, 1990.
[6]  G. Abdel-Aziz, P.-Y. Rescan, B. Clement et al., “Cellular sources of matrix proteins in experimentally induced cholestatic rat liver,” Journal of Pathology, vol. 164, no. 2, pp. 167–174, 1991.
[7]  P. L. Beck and S. S. Lee, “Vitamin K1 improves survival in bile-duct-ligated rats with cirrhosis,” Journal of Hepatology, vol. 23, no. 2, p. 235, 1995.
[8]  K. Yoshioka, A. Mori, K. Taniguchi, and K. Mutoh, “Cell proliferation activity of proliferating bile duct after bile duct ligation in rats,” Veterinary Pathology, vol. 42, no. 3, pp. 382–385, 2005.
[9]  C. Aubé, F. Moal, F. Oberti et al., “Diagnosis and measurement of liver fibrosis by MRI in bile duct ligated rats,” Digestive Diseases and Sciences, vol. 52, no. 10, pp. 2601–2609, 2007.
[10]  H. Zimmermann, H. Blaser, A. Zimmermann, and J. Reichen, “Effect of development on the functional and histological changes induced by bile-duct ligation in the rat,” Journal of Hepatology, vol. 20, no. 2, pp. 231–239, 1994.
[11]  A. M. Gressner and M. G. Bachem, “Molecular mechanisms of liver fibrogenesis: a homage to the role of activated fat-storing cells,” Digestion, vol. 56, no. 5, pp. 335–346, 1995.
[12]  T. Knittel, D. Kobold, F. Piscaglia et al., “Localization of liver myofibroblasts and hepatic stellate cells in normal and diseased rat livers: distinct roles of (myo-)fibroblast subpopulations in hepatic tissue repair,” Histochemistry and Cell Biology, vol. 112, no. 5, pp. 387–401, 1999.
[13]  A. D. Burt, “Cellular and molecular aspects of hepatic fibrosis,” Journal of Pathology, vol. 170, no. 2, pp. 105–115, 1993.
[14]  M. L. Hautekeete and A. Geerts, “The hepatic stellate (Ito) cell: its role in human liver disease,” Virchows Archiv, vol. 430, no. 3, pp. 195–207, 1997.
[15]  M. Zoli, M. R. Cordiani, G. Marchesini et al., “Prognostic indicators in compensated cirrhosis,” The American Journal of Gastroenterology, vol. 86, no. 10, pp. 1508–1513, 1991.
[16]  K. Sekiyama, M. Yoshiba, K. Inoue, and F. Sugata, “Prognostic value of hepatic volumetry in fulminant hepatic failure,” Digestive Diseases and Sciences, vol. 39, no. 2, pp. 240–244, 1994.
[17]  E. Okamoto, N. Yamanaka, T. Oriyama, F. Tomoda, and A. Kyo, “Prediction of the safe limits of hepatectomy by combined volumetric and functional measurements in patients with impaired hepatic function,” Cancer treatment and research, vol. 69, pp. 293–299, 1994.
[18]  P. Soyer, A. Roche, D. Elias, and M. Levesque, “Hepatic metastases from colorectal cancer: influence of hepatic volumetric analysis on surgical decision making,” Radiology, vol. 184, no. 3, pp. 695–697, 1992.
[19]  S. Kawasaki, M. Makuuchi, H. Matsunami et al., “Preoperative measurement of segmental liver volume of donors for living related liver transplantation,” Hepatology, vol. 18, no. 5, pp. 1115–1120, 1993.
[20]  Y. Nakayama, Q. Li, S. Katsuragawa et al., “Automated hepatic volumetry for living related liver transplantation at multisection CT,” Radiology, vol. 240, no. 3, pp. 743–748, 2006.
[21]  K. Kubota, M. Makuuchi, K. Kusaka et al., “Measurement of liver volume and hepatic functional reserve as a guide to decision-making in resectional surgery for hepatic tumors,” Hepatology, vol. 26, no. 5, pp. 1176–1181, 1997.
[22]  I. Birincioglu, S. Topaloglu, N. Turan et al., “Detailed dissection of hepato-caval junction and suprarenal inferior vena cava,” Hepato-Gastroenterology, vol. 58, no. 106, pp. 311–317, 2011.
[23]  Y. Seyama and M. Makuuchi, “Current surgical treatment for bile duct cancer,” World Journal of Gastroenterology, vol. 13, no. 10, pp. 1505–1515, 2007.
[24]  J. M. Regimbeau, D. Fuks, Y.-P. Le Treut et al., “Surgery for hilar cholangiocarcinoma: a multi-institutional update on practice and outcome by the AFC-HC study group,” Journal of Gastrointestinal Surgery, vol. 15, no. 3, pp. 480–488, 2011.
[25]  P. Watanapa, “Recovery patterns of liver function after complete and partial surgical biliary decompression,” The American Journal of Surgery, vol. 171, no. 2, pp. 230–234, 1996.
[26]  V. Singh, V. K. Kapoor, R. Saxena, and S. P. Kaushik, “Recovery of liver functions following surgical biliary decompression in obstructive jaundice,” Hepato-Gastroenterology, vol. 45, no. 22, pp. 1075–1081, 1998.
[27]  P. D. McMaster and P. Rous, “The biliary obstruction required to produce jaundice,” Journal of Experimental Medicine, vol. 33, no. 6, pp. 731–750, 1921.
[28]  N. S. Hadjis, A. Adam, R. Gibson, J. I. Blenkharn, I. S. Benjamin, and L. H. Blumgart, “Nonoperative approach to hilar cancer determined by the atrophy-hypertrophy complex,” The American Journal of Surgery, vol. 157, no. 4, pp. 395–399, 1989.
[29]  T. Noie, Y. Sugawara, H. Imamura, T. Takayama, and M. Makuuchi, “Selective versus total drainage for biliary obstruction in the hepatic hilus: an experimental study,” Surgery, vol. 130, no. 1, pp. 74–81, 2001.

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