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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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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