Eur Surg Res 2014;52:93-250 DOI: 10.1159/000363269 Published online: May 20, 2014
© 2014 S. Karger AG, Basel 0014–312X/14/0524–00093$39.50/0 www.karger.com/esr
The abstracts are available online, free of charge, under www.karger.com/doi/10.1159/000363269
The 49th Congress of the European Society for Surgical Research May 21-24, 2014, Budapest, Hungary
Abstracts Congress Organizing Committee Attila Szijártó, Budapest Péter Ónody, Budapest Prof. Dr. György Wéber, Budapest
94
Walter Brendel Abstracts WB 01_WB 06
97
Young Investigator Abstracts YI 01_YI 06
99
Best Clinical Research Abstracts BC 01_BC 06
102
B.Braun Abstracts YI 01_YI 06
105
Oral Presentations Abstracts OP 01_OP 215
193
Poster Presentations Abstracts PP 01_PP 150
Basel · Freiburg · Paris · London · New York · New Delhi · Bangkok · Beijing · Tokyo · Kuala Lumpur · Singapore · Sydney
Downloaded by: 110.93.234.10 - 5/13/2015 11:57:00 AM
Contents
94
Eur Surg Res 2014;52:93-250 DOI: 10.1159/000363269
Walter Brendel
WB 02
Demonstration of the Effects of Portal Vein Ligation on Clucose Metabolism Using in Vivo Multi-modal Pet/Mri Measurements in Healthy Rat Liver
András Fülöp , András Budai , Viktor Hegedűs , Diana Korsós1, Lászlo Harsányi1, Ildikó Horváth2, Krisztián Szigeti2, Domokos Máthé3, Attila Szijártó1 1
1
1st Department of Surgery, Semmelweis University, Budapest, Hungary 2 Department of Biophysics and Radiation Biology, Semmelweis University, Budapest, Hungary 3 CROmed Translational Research Centers, Budapest, Hungary
1
Background: Portal vein ligation (PVL) results in ipsilateral atrophy and hypertrophy of contralateral liver segments. It is unknown how PVL affects metabolic patterns of hepatic tissues. The aim of this study is to evaluate the effect of PVL on glucose metabolism, using multi-modal PET/MRI imaging in healthy rat liver. Material and Methods: Male Wistar rats (n=30) underwent PVL. 2-deoxy-2-(18F)fluoro-D-glucose (FDG) PET/MRI imaging and morphological/histological examination were performed before; 1-, 2-, 3-, 7-days after PVL. Dynamic PET data were collected and the standardized uptake values (SUV) for ligated and non-ligated liver lobes were calculated in relation to cardiac left ventricle (SUVVOI/SUVCLV) and mean liver SUV (SUVVOI/SUVLiver). Result: PVL induced atrophy of ligated lobes, while non-ligated liver tissue showed compensatory hypertrophy. Dynamic PET scan revealed altered FDG kinetics in both ligated and non-ligated liver lobes. SUVVOI/SUVCLV significantly increased in both groups of lobes, with a maximal value at 2nd postoperative day and returned near to the baseline 7 days after the ligation. After PVL, ligated liver lobes showed significantly higher tracer uptake compared to the non-ligated lobes (significantly higher SUVVOI/SUVLiver values were observed at postoperative day 1, 2 and 3). The homogenous tracer biodistribution observed before PVL reappeared by 7th postoperative day. Conclusion: Our study demonstrated an altered glucose metabolism in both ligated and non-ligated liver lobes. The observed alterations in FDG uptake dynamics should be taken into account during the assessment of PET data until the PVL induced atrophic and regenerative processes are completed.
The Effect of Nitric Oxide Synthase Inhibitor(L-NAME) on Ischemia-reperfusion Injury Following Pringle Maneuver of Cirrhotic Liver Induced by Bile Duct Ligation
Junji Iwasaki1, Mamdouh Afify1, Shinji Uemoto2, Rene H. Tolba1
Institute for Laboratory Animal Science and Experimental Surgery, RWTH-Aachen University, Aachen, Germany 2 Division of Hepatobiliary Pancreatic and Transplant Surgery, Department of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan 1
Background: Pringle maneuver(PM) has been used widely to control blood loss during liver resection. However, hepatic inflow occlusion can also result in hepatic ischemia– reperfusion injury (IRI), especially in patients with a cirrhotic liver. Nitric oxide(NO) is generated from NO synthase(NOS), and has not only cytoprotective but also cytotoxic effect. The aim of this study was to investigate the effect of the NOS inhibitor(L-NAME) on IRI after PM of cirrhotic livers induced by bile duct ligation(BDL). Material and Methods: Male Wistar rats were divided into three groups: sham group(non-BDL/no treatment), L-NAME group(BDL with L-NAME treatment) and BDL group(BDL/no treatment). Cirrhosis was induced by BDL. Two weeks after BDL, 50 % partial hepatectomy with PM was performed. The rats of L-NAME group were injected with L-NAME(1.5 mg/kg) 15 minutes before PM. We evaluated the hepatocellular damage, portal venous flow and microcirculation of the liver after reperfusion. Result: Although there was no significant difference in portal venous flow between L-NAME and BDL group, microcirculation of the liver in L-NAME group tended to be higher than that of BDL group(Table). Histopathologically, the semiquantitative score for liver damage and apoptotic index were significantly lower in L-NAME group than in BDL group 168 hrs after reperfusion. Ki-67 labeling index of L-NAME group was significantly higher than that of BDL group 24 hrs after reperfusion. Conclusion: L-NAME attenuated IRI induced by Pringle maneuver, and improved microcirculation of cirrhotic livers.
Microcirculation flow of the liver (AU)
(Mean ± S.E.M.)
Time after reperfusion (hr)
L-NAME group
24
166.2 ± 30.5
1 3
168
BDL group
226.8 ± 62.2
114.5 ± 7.63
161.3 ± 13.7
94.3 ± 15.2
202.0 ± 73.4
109.5 ± 18.2 125.0 ± 2.65 Downloaded by: 110.93.234.10 - 5/13/2015 11:57:00 AM
WB 01
1
© 2014 S. Karger AG, Basel www.karger.com/esr
95
Eur Surg Res 2014;52:93-250 DOI: 10.1159/000363269
© 2014 S. Karger AG, Basel www.karger.com/esr
WB 03
WB 04
Bacterial Endotoxin Enhances Metastatic Colonisation and Liver Metastasis in Colon Cancer Cells via Nox Derived H2O2
Chemokine Involvement in Lung Injury Secondary to Ischaemia/Reperfusion
1 2
1
2
1
Cork University Hospital, Cork, Ireland University College Cork, Cork, Ireland
Background: Nox-derived reactive oxygen species (ROS) phosphorylate redox sensitive pathways facilitating metastasis. Mediators of surgery-induced inflammation including lipopolysaccharide (LPS) activate Nox enzymes. Surgery-induced inflammation is associated with accelerated tumour growth. Thus we aimed to characterise the potential role for Nox-derived ROS in enhancing metastatic colonisation and liver metastasis in response to LPS. Material and Methods: Balb/C mice underwent an intra-splenic injection of 2x105 pre-treated murine colon cancer CT-26 cells. There were four groups of pre-treated cells – untreated, LPS, LPS + DPI(Nox inhibitor), LPS + DMSO (n=8/ group). Metastatic burden in the liver was assessed by counting surface liver nodules and liver/body weight ratio at day 7 post injection. Mitotic index was assessed using hematoxylin and eosin histology. Metastatic colonisation was assessed in vitro using SW480 cells in migration and invasion assays. ROS characterisation was examined using intracellular probes. Result: LPS treated cells had enhanced liver metastatic burden compared to untreated cells (p=0.036). DPI successfully attenuated metastatic tumour growth compared to untreated and LPS treated groups (p
© 2014 S. Karger AG, Basel 0014–312X/14/0524–00093$39.50/0 www.karger.com/esr
The abstracts are available online, free of charge, under www.karger.com/doi/10.1159/000363269
The 49th Congress of the European Society for Surgical Research May 21-24, 2014, Budapest, Hungary
Abstracts Congress Organizing Committee Attila Szijártó, Budapest Péter Ónody, Budapest Prof. Dr. György Wéber, Budapest
94
Walter Brendel Abstracts WB 01_WB 06
97
Young Investigator Abstracts YI 01_YI 06
99
Best Clinical Research Abstracts BC 01_BC 06
102
B.Braun Abstracts YI 01_YI 06
105
Oral Presentations Abstracts OP 01_OP 215
193
Poster Presentations Abstracts PP 01_PP 150
Basel · Freiburg · Paris · London · New York · New Delhi · Bangkok · Beijing · Tokyo · Kuala Lumpur · Singapore · Sydney
Downloaded by: 110.93.234.10 - 5/13/2015 11:57:00 AM
Contents
94
Eur Surg Res 2014;52:93-250 DOI: 10.1159/000363269
Walter Brendel
WB 02
Demonstration of the Effects of Portal Vein Ligation on Clucose Metabolism Using in Vivo Multi-modal Pet/Mri Measurements in Healthy Rat Liver
András Fülöp , András Budai , Viktor Hegedűs , Diana Korsós1, Lászlo Harsányi1, Ildikó Horváth2, Krisztián Szigeti2, Domokos Máthé3, Attila Szijártó1 1
1
1st Department of Surgery, Semmelweis University, Budapest, Hungary 2 Department of Biophysics and Radiation Biology, Semmelweis University, Budapest, Hungary 3 CROmed Translational Research Centers, Budapest, Hungary
1
Background: Portal vein ligation (PVL) results in ipsilateral atrophy and hypertrophy of contralateral liver segments. It is unknown how PVL affects metabolic patterns of hepatic tissues. The aim of this study is to evaluate the effect of PVL on glucose metabolism, using multi-modal PET/MRI imaging in healthy rat liver. Material and Methods: Male Wistar rats (n=30) underwent PVL. 2-deoxy-2-(18F)fluoro-D-glucose (FDG) PET/MRI imaging and morphological/histological examination were performed before; 1-, 2-, 3-, 7-days after PVL. Dynamic PET data were collected and the standardized uptake values (SUV) for ligated and non-ligated liver lobes were calculated in relation to cardiac left ventricle (SUVVOI/SUVCLV) and mean liver SUV (SUVVOI/SUVLiver). Result: PVL induced atrophy of ligated lobes, while non-ligated liver tissue showed compensatory hypertrophy. Dynamic PET scan revealed altered FDG kinetics in both ligated and non-ligated liver lobes. SUVVOI/SUVCLV significantly increased in both groups of lobes, with a maximal value at 2nd postoperative day and returned near to the baseline 7 days after the ligation. After PVL, ligated liver lobes showed significantly higher tracer uptake compared to the non-ligated lobes (significantly higher SUVVOI/SUVLiver values were observed at postoperative day 1, 2 and 3). The homogenous tracer biodistribution observed before PVL reappeared by 7th postoperative day. Conclusion: Our study demonstrated an altered glucose metabolism in both ligated and non-ligated liver lobes. The observed alterations in FDG uptake dynamics should be taken into account during the assessment of PET data until the PVL induced atrophic and regenerative processes are completed.
The Effect of Nitric Oxide Synthase Inhibitor(L-NAME) on Ischemia-reperfusion Injury Following Pringle Maneuver of Cirrhotic Liver Induced by Bile Duct Ligation
Junji Iwasaki1, Mamdouh Afify1, Shinji Uemoto2, Rene H. Tolba1
Institute for Laboratory Animal Science and Experimental Surgery, RWTH-Aachen University, Aachen, Germany 2 Division of Hepatobiliary Pancreatic and Transplant Surgery, Department of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan 1
Background: Pringle maneuver(PM) has been used widely to control blood loss during liver resection. However, hepatic inflow occlusion can also result in hepatic ischemia– reperfusion injury (IRI), especially in patients with a cirrhotic liver. Nitric oxide(NO) is generated from NO synthase(NOS), and has not only cytoprotective but also cytotoxic effect. The aim of this study was to investigate the effect of the NOS inhibitor(L-NAME) on IRI after PM of cirrhotic livers induced by bile duct ligation(BDL). Material and Methods: Male Wistar rats were divided into three groups: sham group(non-BDL/no treatment), L-NAME group(BDL with L-NAME treatment) and BDL group(BDL/no treatment). Cirrhosis was induced by BDL. Two weeks after BDL, 50 % partial hepatectomy with PM was performed. The rats of L-NAME group were injected with L-NAME(1.5 mg/kg) 15 minutes before PM. We evaluated the hepatocellular damage, portal venous flow and microcirculation of the liver after reperfusion. Result: Although there was no significant difference in portal venous flow between L-NAME and BDL group, microcirculation of the liver in L-NAME group tended to be higher than that of BDL group(Table). Histopathologically, the semiquantitative score for liver damage and apoptotic index were significantly lower in L-NAME group than in BDL group 168 hrs after reperfusion. Ki-67 labeling index of L-NAME group was significantly higher than that of BDL group 24 hrs after reperfusion. Conclusion: L-NAME attenuated IRI induced by Pringle maneuver, and improved microcirculation of cirrhotic livers.
Microcirculation flow of the liver (AU)
(Mean ± S.E.M.)
Time after reperfusion (hr)
L-NAME group
24
166.2 ± 30.5
1 3
168
BDL group
226.8 ± 62.2
114.5 ± 7.63
161.3 ± 13.7
94.3 ± 15.2
202.0 ± 73.4
109.5 ± 18.2 125.0 ± 2.65 Downloaded by: 110.93.234.10 - 5/13/2015 11:57:00 AM
WB 01
1
© 2014 S. Karger AG, Basel www.karger.com/esr
95
Eur Surg Res 2014;52:93-250 DOI: 10.1159/000363269
© 2014 S. Karger AG, Basel www.karger.com/esr
WB 03
WB 04
Bacterial Endotoxin Enhances Metastatic Colonisation and Liver Metastasis in Colon Cancer Cells via Nox Derived H2O2
Chemokine Involvement in Lung Injury Secondary to Ischaemia/Reperfusion
1 2
1
2
1
Cork University Hospital, Cork, Ireland University College Cork, Cork, Ireland
Background: Nox-derived reactive oxygen species (ROS) phosphorylate redox sensitive pathways facilitating metastasis. Mediators of surgery-induced inflammation including lipopolysaccharide (LPS) activate Nox enzymes. Surgery-induced inflammation is associated with accelerated tumour growth. Thus we aimed to characterise the potential role for Nox-derived ROS in enhancing metastatic colonisation and liver metastasis in response to LPS. Material and Methods: Balb/C mice underwent an intra-splenic injection of 2x105 pre-treated murine colon cancer CT-26 cells. There were four groups of pre-treated cells – untreated, LPS, LPS + DPI(Nox inhibitor), LPS + DMSO (n=8/ group). Metastatic burden in the liver was assessed by counting surface liver nodules and liver/body weight ratio at day 7 post injection. Mitotic index was assessed using hematoxylin and eosin histology. Metastatic colonisation was assessed in vitro using SW480 cells in migration and invasion assays. ROS characterisation was examined using intracellular probes. Result: LPS treated cells had enhanced liver metastatic burden compared to untreated cells (p=0.036). DPI successfully attenuated metastatic tumour growth compared to untreated and LPS treated groups (p
