The effects of hemorrhagic shock secondary to hepatectomy in a swine model

Abstract Background Ischemia–reperfusion injury caused by severe hemorrhagic shock and subsequent resuscitation leads to deterioration of hepatic homeostasis and possibly to liver failure. The present study focuses on determining whether there is a different biological response to hemorrhagic shock...

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Veröffentlicht in:The Journal of surgical research 2015-05, Vol.195 (1), p.228-234
Hauptverfasser: Mylonas, Anastasios I., MD, Orfanos, Nikolaos F., MD, Karmaniolou, Iosifina I., MD, PhD, DESA, Lolis, Evangelos D., MD, PhD, Stergiou, Eirini P, Papalois, Apostolos E., PhD, Nomikos, Tzortzis N., PhD, Kondi-Pafiti, Agathi I., MD, PhD, Smyrniotis, Vasileios E., MD, PhD, Arkadopoulos, Nikolaos F., MD, PhD
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container_issue 1
container_start_page 228
container_title The Journal of surgical research
container_volume 195
creator Mylonas, Anastasios I., MD
Orfanos, Nikolaos F., MD
Karmaniolou, Iosifina I., MD, PhD, DESA
Lolis, Evangelos D., MD, PhD
Stergiou, Eirini P
Papalois, Apostolos E., PhD
Nomikos, Tzortzis N., PhD
Kondi-Pafiti, Agathi I., MD, PhD
Smyrniotis, Vasileios E., MD, PhD
Arkadopoulos, Nikolaos F., MD, PhD
description Abstract Background Ischemia–reperfusion injury caused by severe hemorrhagic shock and subsequent resuscitation leads to deterioration of hepatic homeostasis and possibly to liver failure. The present study focuses on determining whether there is a different biological response to hemorrhagic shock by different sources of hemorrhage, hepatic hemorrhage (HH) versus peripheral hemorrhage. Methods Twenty-one male swine (Sus scrofa domesticus) were randomly allocated in three groups as follows: sham group (S, n  = 5), central venous hemorrhage group, (CVH) ( n  = 8), and HH group ( n  = 8). Hepatectomy of the left liver lobe was carried out in groups CVH and HH, and the animals were subjected to controlled bleeding from the internal jugular vein and the traumatic liver surface, respectively. After 10 min of hemorrhage, shock was maintained for 30 min at mean arterial pressure levels of 30 mm Hg–40 mm Hg and resuscitation was initiated with crystalloids and colloids. Hemodynamic parameters and fluid balance were monitored throughout the 6 h of total duration of the experiment. Blood samples were collected at 0-, 40-, and 360-min time points for transaminases, albumin, and interleukin-6 measurement. Hepatic tissue was harvested at the end of the experiment for oxidative marker and proliferation analysis. Results Although blood loss was comparable between the two groups, the amount of fluids needed for resuscitation was higher for the HH group. Inflammatory response, measured by interleukin-6, was found higher in HH group. Oxidative stress markers did not reveal statistically significant difference between the two groups. Liver hemorrhage decreased hepatocellular proliferation measured by proliferating cell nuclear antigen. Conclusions Our study provides evidence that HH entails worse consequences for the hepatocytes than systemic hemorrhage. Higher needs for resuscitation fluids, decreased proliferation, and augmented inflammatory response when HH takes place are findings with possible clinical importance in liver surgery and trauma.
doi_str_mv 10.1016/j.jss.2014.12.046
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The present study focuses on determining whether there is a different biological response to hemorrhagic shock by different sources of hemorrhage, hepatic hemorrhage (HH) versus peripheral hemorrhage. Methods Twenty-one male swine (Sus scrofa domesticus) were randomly allocated in three groups as follows: sham group (S, n  = 5), central venous hemorrhage group, (CVH) ( n  = 8), and HH group ( n  = 8). Hepatectomy of the left liver lobe was carried out in groups CVH and HH, and the animals were subjected to controlled bleeding from the internal jugular vein and the traumatic liver surface, respectively. After 10 min of hemorrhage, shock was maintained for 30 min at mean arterial pressure levels of 30 mm Hg–40 mm Hg and resuscitation was initiated with crystalloids and colloids. Hemodynamic parameters and fluid balance were monitored throughout the 6 h of total duration of the experiment. Blood samples were collected at 0-, 40-, and 360-min time points for transaminases, albumin, and interleukin-6 measurement. Hepatic tissue was harvested at the end of the experiment for oxidative marker and proliferation analysis. Results Although blood loss was comparable between the two groups, the amount of fluids needed for resuscitation was higher for the HH group. Inflammatory response, measured by interleukin-6, was found higher in HH group. Oxidative stress markers did not reveal statistically significant difference between the two groups. Liver hemorrhage decreased hepatocellular proliferation measured by proliferating cell nuclear antigen. Conclusions Our study provides evidence that HH entails worse consequences for the hepatocytes than systemic hemorrhage. Higher needs for resuscitation fluids, decreased proliferation, and augmented inflammatory response when HH takes place are findings with possible clinical importance in liver surgery and trauma.</description><identifier>ISSN: 0022-4804</identifier><identifier>EISSN: 1095-8673</identifier><identifier>DOI: 10.1016/j.jss.2014.12.046</identifier><identifier>PMID: 25659614</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Blood Loss, Surgical ; Central venous hemorrhage ; Disease Models, Animal ; Hemodynamics ; Hepatectomy - adverse effects ; Hepatic hemorrhage ; Hepatocyte proliferation ; Interleukin 6 ; Ischemia–reperfusion ; Liver - metabolism ; Liver - pathology ; Male ; Postoperative Complications - etiology ; Postoperative Complications - metabolism ; Postoperative Complications - pathology ; Postoperative Complications - therapy ; Random Allocation ; Resuscitation ; Shock, Hemorrhagic - etiology ; Shock, Hemorrhagic - metabolism ; Shock, Hemorrhagic - pathology ; Shock, Hemorrhagic - therapy ; Surgery ; Swine</subject><ispartof>The Journal of surgical research, 2015-05, Vol.195 (1), p.228-234</ispartof><rights>Elsevier Inc.</rights><rights>2015 Elsevier Inc.</rights><rights>Copyright © 2015 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-89592179c110c992d2d27460b877bb83f7fc6397f87cb10efb6ade5ed3d75cd93</citedby><cites>FETCH-LOGICAL-c408t-89592179c110c992d2d27460b877bb83f7fc6397f87cb10efb6ade5ed3d75cd93</cites><orcidid>0000-0003-0402-378X ; 0000-0003-2492-6396</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jss.2014.12.046$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25659614$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mylonas, Anastasios I., MD</creatorcontrib><creatorcontrib>Orfanos, Nikolaos F., MD</creatorcontrib><creatorcontrib>Karmaniolou, Iosifina I., MD, PhD, DESA</creatorcontrib><creatorcontrib>Lolis, Evangelos D., MD, PhD</creatorcontrib><creatorcontrib>Stergiou, Eirini P</creatorcontrib><creatorcontrib>Papalois, Apostolos E., PhD</creatorcontrib><creatorcontrib>Nomikos, Tzortzis N., PhD</creatorcontrib><creatorcontrib>Kondi-Pafiti, Agathi I., MD, PhD</creatorcontrib><creatorcontrib>Smyrniotis, Vasileios E., MD, PhD</creatorcontrib><creatorcontrib>Arkadopoulos, Nikolaos F., MD, PhD</creatorcontrib><title>The effects of hemorrhagic shock secondary to hepatectomy in a swine model</title><title>The Journal of surgical research</title><addtitle>J Surg Res</addtitle><description>Abstract Background Ischemia–reperfusion injury caused by severe hemorrhagic shock and subsequent resuscitation leads to deterioration of hepatic homeostasis and possibly to liver failure. The present study focuses on determining whether there is a different biological response to hemorrhagic shock by different sources of hemorrhage, hepatic hemorrhage (HH) versus peripheral hemorrhage. Methods Twenty-one male swine (Sus scrofa domesticus) were randomly allocated in three groups as follows: sham group (S, n  = 5), central venous hemorrhage group, (CVH) ( n  = 8), and HH group ( n  = 8). Hepatectomy of the left liver lobe was carried out in groups CVH and HH, and the animals were subjected to controlled bleeding from the internal jugular vein and the traumatic liver surface, respectively. After 10 min of hemorrhage, shock was maintained for 30 min at mean arterial pressure levels of 30 mm Hg–40 mm Hg and resuscitation was initiated with crystalloids and colloids. Hemodynamic parameters and fluid balance were monitored throughout the 6 h of total duration of the experiment. Blood samples were collected at 0-, 40-, and 360-min time points for transaminases, albumin, and interleukin-6 measurement. Hepatic tissue was harvested at the end of the experiment for oxidative marker and proliferation analysis. Results Although blood loss was comparable between the two groups, the amount of fluids needed for resuscitation was higher for the HH group. Inflammatory response, measured by interleukin-6, was found higher in HH group. Oxidative stress markers did not reveal statistically significant difference between the two groups. Liver hemorrhage decreased hepatocellular proliferation measured by proliferating cell nuclear antigen. Conclusions Our study provides evidence that HH entails worse consequences for the hepatocytes than systemic hemorrhage. Higher needs for resuscitation fluids, decreased proliferation, and augmented inflammatory response when HH takes place are findings with possible clinical importance in liver surgery and trauma.</description><subject>Animals</subject><subject>Blood Loss, Surgical</subject><subject>Central venous hemorrhage</subject><subject>Disease Models, Animal</subject><subject>Hemodynamics</subject><subject>Hepatectomy - adverse effects</subject><subject>Hepatic hemorrhage</subject><subject>Hepatocyte proliferation</subject><subject>Interleukin 6</subject><subject>Ischemia–reperfusion</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Male</subject><subject>Postoperative Complications - etiology</subject><subject>Postoperative Complications - metabolism</subject><subject>Postoperative Complications - pathology</subject><subject>Postoperative Complications - therapy</subject><subject>Random Allocation</subject><subject>Resuscitation</subject><subject>Shock, Hemorrhagic - etiology</subject><subject>Shock, Hemorrhagic - metabolism</subject><subject>Shock, Hemorrhagic - pathology</subject><subject>Shock, Hemorrhagic - therapy</subject><subject>Surgery</subject><subject>Swine</subject><issn>0022-4804</issn><issn>1095-8673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcFq3DAURUVpaCZJP6CbomU3dvRkW7IoFEpom4RAFknWwpaeOnJsayJ5Wubvo2HSLLoIWgihcy-88wj5BKwEBuJ8KIeUSs6gLoGXrBbvyAqYaopWyOo9WTHGeVG3rD4mJykNLL-VrD6QY96IRgmoV-T6fo0UnUOzJBocXeMUYlx3v72haR3MI01owmy7uKNLyN-bbslsmHbUz7Sj6a-fkU7B4nhGjlw3Jvz4cp-Sh58_7i8ui5vbX1cX328KU7N2KVrVKA5SGQBmlOI2H1kL1rdS9n1bOemMqJR0rTQ9MHS96Cw2aCsrG2NVdUq-HHo3MTxtMS168sngOHYzhm3SICRwaBSDjMIBNTGkFNHpTfRTnkUD03uFetBZod4r1MB1Vpgzn1_qt_2E9jXxz1kGvh4AzEP-8Rh1Mh5ng9bHrEbb4N-s__Zf2ox-9qYbH3GHaQjbOGd7GnTKAX233-F-hVAzAMFl9Qyp4JXy</recordid><startdate>20150501</startdate><enddate>20150501</enddate><creator>Mylonas, Anastasios I., MD</creator><creator>Orfanos, Nikolaos F., MD</creator><creator>Karmaniolou, Iosifina I., MD, PhD, DESA</creator><creator>Lolis, Evangelos D., MD, PhD</creator><creator>Stergiou, Eirini P</creator><creator>Papalois, Apostolos E., PhD</creator><creator>Nomikos, Tzortzis N., PhD</creator><creator>Kondi-Pafiti, Agathi I., MD, PhD</creator><creator>Smyrniotis, Vasileios E., MD, PhD</creator><creator>Arkadopoulos, Nikolaos F., MD, PhD</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-0402-378X</orcidid><orcidid>https://orcid.org/0000-0003-2492-6396</orcidid></search><sort><creationdate>20150501</creationdate><title>The effects of hemorrhagic shock secondary to hepatectomy in a swine model</title><author>Mylonas, Anastasios I., MD ; Orfanos, Nikolaos F., MD ; Karmaniolou, Iosifina I., MD, PhD, DESA ; Lolis, Evangelos D., MD, PhD ; Stergiou, Eirini P ; Papalois, Apostolos E., PhD ; Nomikos, Tzortzis N., PhD ; Kondi-Pafiti, Agathi I., MD, PhD ; Smyrniotis, Vasileios E., MD, PhD ; Arkadopoulos, Nikolaos F., MD, PhD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-89592179c110c992d2d27460b877bb83f7fc6397f87cb10efb6ade5ed3d75cd93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Blood Loss, Surgical</topic><topic>Central venous hemorrhage</topic><topic>Disease Models, Animal</topic><topic>Hemodynamics</topic><topic>Hepatectomy - adverse effects</topic><topic>Hepatic hemorrhage</topic><topic>Hepatocyte proliferation</topic><topic>Interleukin 6</topic><topic>Ischemia–reperfusion</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Male</topic><topic>Postoperative Complications - etiology</topic><topic>Postoperative Complications - metabolism</topic><topic>Postoperative Complications - pathology</topic><topic>Postoperative Complications - therapy</topic><topic>Random Allocation</topic><topic>Resuscitation</topic><topic>Shock, Hemorrhagic - etiology</topic><topic>Shock, Hemorrhagic - metabolism</topic><topic>Shock, Hemorrhagic - pathology</topic><topic>Shock, Hemorrhagic - therapy</topic><topic>Surgery</topic><topic>Swine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mylonas, Anastasios I., MD</creatorcontrib><creatorcontrib>Orfanos, Nikolaos F., MD</creatorcontrib><creatorcontrib>Karmaniolou, Iosifina I., MD, PhD, DESA</creatorcontrib><creatorcontrib>Lolis, Evangelos D., MD, PhD</creatorcontrib><creatorcontrib>Stergiou, Eirini P</creatorcontrib><creatorcontrib>Papalois, Apostolos E., PhD</creatorcontrib><creatorcontrib>Nomikos, Tzortzis N., PhD</creatorcontrib><creatorcontrib>Kondi-Pafiti, Agathi I., MD, PhD</creatorcontrib><creatorcontrib>Smyrniotis, Vasileios E., MD, PhD</creatorcontrib><creatorcontrib>Arkadopoulos, Nikolaos F., MD, PhD</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of surgical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mylonas, Anastasios I., MD</au><au>Orfanos, Nikolaos F., MD</au><au>Karmaniolou, Iosifina I., MD, PhD, DESA</au><au>Lolis, Evangelos D., MD, PhD</au><au>Stergiou, Eirini P</au><au>Papalois, Apostolos E., PhD</au><au>Nomikos, Tzortzis N., PhD</au><au>Kondi-Pafiti, Agathi I., MD, PhD</au><au>Smyrniotis, Vasileios E., MD, PhD</au><au>Arkadopoulos, Nikolaos F., MD, PhD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The effects of hemorrhagic shock secondary to hepatectomy in a swine model</atitle><jtitle>The Journal of surgical research</jtitle><addtitle>J Surg Res</addtitle><date>2015-05-01</date><risdate>2015</risdate><volume>195</volume><issue>1</issue><spage>228</spage><epage>234</epage><pages>228-234</pages><issn>0022-4804</issn><eissn>1095-8673</eissn><abstract>Abstract Background Ischemia–reperfusion injury caused by severe hemorrhagic shock and subsequent resuscitation leads to deterioration of hepatic homeostasis and possibly to liver failure. The present study focuses on determining whether there is a different biological response to hemorrhagic shock by different sources of hemorrhage, hepatic hemorrhage (HH) versus peripheral hemorrhage. Methods Twenty-one male swine (Sus scrofa domesticus) were randomly allocated in three groups as follows: sham group (S, n  = 5), central venous hemorrhage group, (CVH) ( n  = 8), and HH group ( n  = 8). Hepatectomy of the left liver lobe was carried out in groups CVH and HH, and the animals were subjected to controlled bleeding from the internal jugular vein and the traumatic liver surface, respectively. After 10 min of hemorrhage, shock was maintained for 30 min at mean arterial pressure levels of 30 mm Hg–40 mm Hg and resuscitation was initiated with crystalloids and colloids. Hemodynamic parameters and fluid balance were monitored throughout the 6 h of total duration of the experiment. Blood samples were collected at 0-, 40-, and 360-min time points for transaminases, albumin, and interleukin-6 measurement. Hepatic tissue was harvested at the end of the experiment for oxidative marker and proliferation analysis. Results Although blood loss was comparable between the two groups, the amount of fluids needed for resuscitation was higher for the HH group. Inflammatory response, measured by interleukin-6, was found higher in HH group. Oxidative stress markers did not reveal statistically significant difference between the two groups. Liver hemorrhage decreased hepatocellular proliferation measured by proliferating cell nuclear antigen. Conclusions Our study provides evidence that HH entails worse consequences for the hepatocytes than systemic hemorrhage. Higher needs for resuscitation fluids, decreased proliferation, and augmented inflammatory response when HH takes place are findings with possible clinical importance in liver surgery and trauma.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>25659614</pmid><doi>10.1016/j.jss.2014.12.046</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0003-0402-378X</orcidid><orcidid>https://orcid.org/0000-0003-2492-6396</orcidid></addata></record>
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subjects Animals
Blood Loss, Surgical
Central venous hemorrhage
Disease Models, Animal
Hemodynamics
Hepatectomy - adverse effects
Hepatic hemorrhage
Hepatocyte proliferation
Interleukin 6
Ischemia–reperfusion
Liver - metabolism
Liver - pathology
Male
Postoperative Complications - etiology
Postoperative Complications - metabolism
Postoperative Complications - pathology
Postoperative Complications - therapy
Random Allocation
Resuscitation
Shock, Hemorrhagic - etiology
Shock, Hemorrhagic - metabolism
Shock, Hemorrhagic - pathology
Shock, Hemorrhagic - therapy
Surgery
Swine
title The effects of hemorrhagic shock secondary to hepatectomy in a swine model
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