Effects of heme oxygenase-1 on pulmonary function and structure in rats with liver cirrhosis

Background The hepatopulmonary syndrome (HPS) is a severe vascular complication in lungs resulting in systemic hypoxemia in patients with cirrhosis and portal hypertension. The underlying structural change in HPS is intrapulmonary vasodilation, which can lead to impaired oxygenation of pulmonary ven...

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Veröffentlicht in:Chinese medical journal 2011-03, Vol.124 (6), p.918-922
Hauptverfasser: Guo, Shi-bin, Duan, Zhi-jun, Li, Qing, Sun, Xiao-yu
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Duan, Zhi-jun
Li, Qing
Sun, Xiao-yu
description Background The hepatopulmonary syndrome (HPS) is a severe vascular complication in lungs resulting in systemic hypoxemia in patients with cirrhosis and portal hypertension. The underlying structural change in HPS is intrapulmonary vasodilation, which can lead to impaired oxygenation of pulmonary venous blood. It has been demonstrated that the heme oxygenase-1/carbon monoxide (HO-1/CO) system plays an important role in the control of vascular tone. The aim of this study was to further investigate the role of HO-1 in the pathogenesis of HPS in animal model.Methods Totally 35 rats were divided into liver cirrhosis, zinc protoporphyrin Ⅸ (ZnPP), cobalt protoporphyrin (CoPP)and sham groups. Biliary cirrhosis was established in the first three groups by bile duct ligation. Rats in the ZnPP and CoPP groups received once intraperitoneal injection of ZnPP and CoPP, respectively, 24 hours before sample collection.Expression of HO-1 mRNA in lung was detected by reverse-transcription polymerase chain reaction, while protein expression was determined by immunohistochemical analysis. Hematoxylin and eosin staining was performed to confirm the presence of liver cirrhosis and intrapulmonary vasodilation. Arterial blood gases, mean arterial pressure and portal vein pressure were also measured. Analysis of variance or Wilcoxon statistical methods were used to determine statistical significance.Results Compared with the sham group, the cirrhotic group demonstrated increased expression of pulmonary HO-1 mRNA and protein (P〈0.01). The level of arterial carboxyhemoglobin (COHb), alveolar-arterial oxygen gradient (A-aPO2),mean arterial pressure, portal vein pressure (P〈0.05, respectively), and intrapulmonary vasodilation were also significantly increased. Compared with the cirrhotic group, CoPP treatment increased pulmonary HO-1 mRNA and protein expression, the level of A-aPO2 (P 〈0.05 respectively), COHb (P 〈0.01), and intrapulmonary vasodilation, while ZnPP treatment decreased pulmonary HO-1 mRNA and protein expression, the level of COHb (P 〈0.05 respectively),and intrapulmonary vasodilation, without obvious alteration of mean arterial pressure and portal vein pressure.Conclusion Increased pulmonary HO-1 expression is an important contributor to the development of experimental HPS.
doi_str_mv 10.3760/cma.j.issn.0366-6999.2011.06.021
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fullrecord <record><control><sourceid>wanfang_jour_proqu</sourceid><recordid>TN_cdi_wanfang_journals_zhcmj201106021</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><cqvip_id>37587405</cqvip_id><wanfj_id>zhcmj201106021</wanfj_id><sourcerecordid>zhcmj201106021</sourcerecordid><originalsourceid>FETCH-LOGICAL-c1831-e448e008fc9467c7eb446803297e0b86ece03f40df47f1085ec1f4db7258a52b3</originalsourceid><addsrcrecordid>eNo90E1v1DAQgGELgehS-AvI4gBcEsbfzhFV5UOqxAVuSJHjHW-8JM7WTijl12O0hdNIo8ce6SXkLYNWGA3v_OzaYxtLSS0IrRvddV3LgbEWdAucPSI7riRvlJbsMdn9NxfkWSlHAK6U0U_JBWeKWQ1iR75fh4B-LXQJdMQZ6fLr_oDJFWwYXRI9bdO8JJfvadiSX2NdubSnZc2bX7eMNCaaXX1_F9eRTvEnZupjzuNSYnlOngQ3FXzxMC_Jtw_XX68-NTdfPn6-en_TeGYFa1BKiwA2-E5q4w0OUmoLgncGYbAaPYIIEvZBmsDAKvQsyP1guLJO8UFcktfnf-9cCi4d-uOy5VQv9r9HPx__BgJd81T45gxPebndsKz9HIvHaXIJl630VtfMnZCiypcPchtm3PenHOdaof9XroJXZ-DHJR1uY706OP8jxAl7YZQ1EpT4A79ef8I</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>863769343</pqid></control><display><type>article</type><title>Effects of heme oxygenase-1 on pulmonary function and structure in rats with liver cirrhosis</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Guo, Shi-bin ; Duan, Zhi-jun ; Li, Qing ; Sun, Xiao-yu</creator><creatorcontrib>Guo, Shi-bin ; Duan, Zhi-jun ; Li, Qing ; Sun, Xiao-yu</creatorcontrib><description>Background The hepatopulmonary syndrome (HPS) is a severe vascular complication in lungs resulting in systemic hypoxemia in patients with cirrhosis and portal hypertension. The underlying structural change in HPS is intrapulmonary vasodilation, which can lead to impaired oxygenation of pulmonary venous blood. It has been demonstrated that the heme oxygenase-1/carbon monoxide (HO-1/CO) system plays an important role in the control of vascular tone. The aim of this study was to further investigate the role of HO-1 in the pathogenesis of HPS in animal model.Methods Totally 35 rats were divided into liver cirrhosis, zinc protoporphyrin Ⅸ (ZnPP), cobalt protoporphyrin (CoPP)and sham groups. Biliary cirrhosis was established in the first three groups by bile duct ligation. Rats in the ZnPP and CoPP groups received once intraperitoneal injection of ZnPP and CoPP, respectively, 24 hours before sample collection.Expression of HO-1 mRNA in lung was detected by reverse-transcription polymerase chain reaction, while protein expression was determined by immunohistochemical analysis. Hematoxylin and eosin staining was performed to confirm the presence of liver cirrhosis and intrapulmonary vasodilation. Arterial blood gases, mean arterial pressure and portal vein pressure were also measured. Analysis of variance or Wilcoxon statistical methods were used to determine statistical significance.Results Compared with the sham group, the cirrhotic group demonstrated increased expression of pulmonary HO-1 mRNA and protein (P〈0.01). The level of arterial carboxyhemoglobin (COHb), alveolar-arterial oxygen gradient (A-aPO2),mean arterial pressure, portal vein pressure (P〈0.05, respectively), and intrapulmonary vasodilation were also significantly increased. Compared with the cirrhotic group, CoPP treatment increased pulmonary HO-1 mRNA and protein expression, the level of A-aPO2 (P 〈0.05 respectively), COHb (P 〈0.01), and intrapulmonary vasodilation, while ZnPP treatment decreased pulmonary HO-1 mRNA and protein expression, the level of COHb (P 〈0.05 respectively),and intrapulmonary vasodilation, without obvious alteration of mean arterial pressure and portal vein pressure.Conclusion Increased pulmonary HO-1 expression is an important contributor to the development of experimental HPS.</description><identifier>ISSN: 0366-6999</identifier><identifier>EISSN: 2542-5641</identifier><identifier>DOI: 10.3760/cma.j.issn.0366-6999.2011.06.021</identifier><identifier>PMID: 21518603</identifier><language>eng</language><publisher>China: Department of Gastroenterology, First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116001, China</publisher><subject>Animals ; Enzyme Inhibitors - therapeutic use ; Heme Oxygenase-1 - genetics ; Heme Oxygenase-1 - metabolism ; Hemodynamics ; Immunohistochemistry ; Liver Cirrhosis - enzymology ; Liver Cirrhosis - genetics ; Lung - drug effects ; Lung - metabolism ; Male ; mRNA表达 ; Protoporphyrins - therapeutic use ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; 平均动脉压 ; 本结构 ; 肝硬化 ; 肺功能 ; 血红素氧化酶 ; 逆转录聚合酶链反应</subject><ispartof>Chinese medical journal, 2011-03, Vol.124 (6), p.918-922</ispartof><rights>Copyright © Wanfang Data Co. Ltd. All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/85656X/85656X.jpg</thumbnail><link.rule.ids>314,780,784,864,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21518603$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Shi-bin</creatorcontrib><creatorcontrib>Duan, Zhi-jun</creatorcontrib><creatorcontrib>Li, Qing</creatorcontrib><creatorcontrib>Sun, Xiao-yu</creatorcontrib><title>Effects of heme oxygenase-1 on pulmonary function and structure in rats with liver cirrhosis</title><title>Chinese medical journal</title><addtitle>Chinese Medical Journal</addtitle><description>Background The hepatopulmonary syndrome (HPS) is a severe vascular complication in lungs resulting in systemic hypoxemia in patients with cirrhosis and portal hypertension. The underlying structural change in HPS is intrapulmonary vasodilation, which can lead to impaired oxygenation of pulmonary venous blood. It has been demonstrated that the heme oxygenase-1/carbon monoxide (HO-1/CO) system plays an important role in the control of vascular tone. The aim of this study was to further investigate the role of HO-1 in the pathogenesis of HPS in animal model.Methods Totally 35 rats were divided into liver cirrhosis, zinc protoporphyrin Ⅸ (ZnPP), cobalt protoporphyrin (CoPP)and sham groups. Biliary cirrhosis was established in the first three groups by bile duct ligation. Rats in the ZnPP and CoPP groups received once intraperitoneal injection of ZnPP and CoPP, respectively, 24 hours before sample collection.Expression of HO-1 mRNA in lung was detected by reverse-transcription polymerase chain reaction, while protein expression was determined by immunohistochemical analysis. Hematoxylin and eosin staining was performed to confirm the presence of liver cirrhosis and intrapulmonary vasodilation. Arterial blood gases, mean arterial pressure and portal vein pressure were also measured. Analysis of variance or Wilcoxon statistical methods were used to determine statistical significance.Results Compared with the sham group, the cirrhotic group demonstrated increased expression of pulmonary HO-1 mRNA and protein (P〈0.01). The level of arterial carboxyhemoglobin (COHb), alveolar-arterial oxygen gradient (A-aPO2),mean arterial pressure, portal vein pressure (P〈0.05, respectively), and intrapulmonary vasodilation were also significantly increased. Compared with the cirrhotic group, CoPP treatment increased pulmonary HO-1 mRNA and protein expression, the level of A-aPO2 (P 〈0.05 respectively), COHb (P 〈0.01), and intrapulmonary vasodilation, while ZnPP treatment decreased pulmonary HO-1 mRNA and protein expression, the level of COHb (P 〈0.05 respectively),and intrapulmonary vasodilation, without obvious alteration of mean arterial pressure and portal vein pressure.Conclusion Increased pulmonary HO-1 expression is an important contributor to the development of experimental HPS.</description><subject>Animals</subject><subject>Enzyme Inhibitors - therapeutic use</subject><subject>Heme Oxygenase-1 - genetics</subject><subject>Heme Oxygenase-1 - metabolism</subject><subject>Hemodynamics</subject><subject>Immunohistochemistry</subject><subject>Liver Cirrhosis - enzymology</subject><subject>Liver Cirrhosis - genetics</subject><subject>Lung - drug effects</subject><subject>Lung - metabolism</subject><subject>Male</subject><subject>mRNA表达</subject><subject>Protoporphyrins - therapeutic use</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>平均动脉压</subject><subject>本结构</subject><subject>肝硬化</subject><subject>肺功能</subject><subject>血红素氧化酶</subject><subject>逆转录聚合酶链反应</subject><issn>0366-6999</issn><issn>2542-5641</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo90E1v1DAQgGELgehS-AvI4gBcEsbfzhFV5UOqxAVuSJHjHW-8JM7WTijl12O0hdNIo8ce6SXkLYNWGA3v_OzaYxtLSS0IrRvddV3LgbEWdAucPSI7riRvlJbsMdn9NxfkWSlHAK6U0U_JBWeKWQ1iR75fh4B-LXQJdMQZ6fLr_oDJFWwYXRI9bdO8JJfvadiSX2NdubSnZc2bX7eMNCaaXX1_F9eRTvEnZupjzuNSYnlOngQ3FXzxMC_Jtw_XX68-NTdfPn6-en_TeGYFa1BKiwA2-E5q4w0OUmoLgncGYbAaPYIIEvZBmsDAKvQsyP1guLJO8UFcktfnf-9cCi4d-uOy5VQv9r9HPx__BgJd81T45gxPebndsKz9HIvHaXIJl630VtfMnZCiypcPchtm3PenHOdaof9XroJXZ-DHJR1uY706OP8jxAl7YZQ1EpT4A79ef8I</recordid><startdate>201103</startdate><enddate>201103</enddate><creator>Guo, Shi-bin</creator><creator>Duan, Zhi-jun</creator><creator>Li, Qing</creator><creator>Sun, Xiao-yu</creator><general>Department of Gastroenterology, First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116001, China</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W95</scope><scope>~WA</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>2B.</scope><scope>4A8</scope><scope>92I</scope><scope>93N</scope><scope>PSX</scope><scope>TCJ</scope></search><sort><creationdate>201103</creationdate><title>Effects of heme oxygenase-1 on pulmonary function and structure in rats with liver cirrhosis</title><author>Guo, Shi-bin ; Duan, Zhi-jun ; Li, Qing ; Sun, Xiao-yu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1831-e448e008fc9467c7eb446803297e0b86ece03f40df47f1085ec1f4db7258a52b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Enzyme Inhibitors - therapeutic use</topic><topic>Heme Oxygenase-1 - genetics</topic><topic>Heme Oxygenase-1 - metabolism</topic><topic>Hemodynamics</topic><topic>Immunohistochemistry</topic><topic>Liver Cirrhosis - enzymology</topic><topic>Liver Cirrhosis - genetics</topic><topic>Lung - drug effects</topic><topic>Lung - metabolism</topic><topic>Male</topic><topic>mRNA表达</topic><topic>Protoporphyrins - therapeutic use</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>平均动脉压</topic><topic>本结构</topic><topic>肝硬化</topic><topic>肺功能</topic><topic>血红素氧化酶</topic><topic>逆转录聚合酶链反应</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guo, Shi-bin</creatorcontrib><creatorcontrib>Duan, Zhi-jun</creatorcontrib><creatorcontrib>Li, Qing</creatorcontrib><creatorcontrib>Sun, Xiao-yu</creatorcontrib><collection>中文科技期刊数据库</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库-农业科学</collection><collection>中文科技期刊数据库- 镜像站点</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>Wanfang Data Journals - Hong Kong</collection><collection>WANFANG Data Centre</collection><collection>Wanfang Data Journals</collection><collection>万方数据期刊 - 香港版</collection><collection>China Online Journals (COJ)</collection><collection>China Online Journals (COJ)</collection><jtitle>Chinese medical journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, Shi-bin</au><au>Duan, Zhi-jun</au><au>Li, Qing</au><au>Sun, Xiao-yu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of heme oxygenase-1 on pulmonary function and structure in rats with liver cirrhosis</atitle><jtitle>Chinese medical journal</jtitle><addtitle>Chinese Medical Journal</addtitle><date>2011-03</date><risdate>2011</risdate><volume>124</volume><issue>6</issue><spage>918</spage><epage>922</epage><pages>918-922</pages><issn>0366-6999</issn><eissn>2542-5641</eissn><abstract>Background The hepatopulmonary syndrome (HPS) is a severe vascular complication in lungs resulting in systemic hypoxemia in patients with cirrhosis and portal hypertension. The underlying structural change in HPS is intrapulmonary vasodilation, which can lead to impaired oxygenation of pulmonary venous blood. It has been demonstrated that the heme oxygenase-1/carbon monoxide (HO-1/CO) system plays an important role in the control of vascular tone. The aim of this study was to further investigate the role of HO-1 in the pathogenesis of HPS in animal model.Methods Totally 35 rats were divided into liver cirrhosis, zinc protoporphyrin Ⅸ (ZnPP), cobalt protoporphyrin (CoPP)and sham groups. Biliary cirrhosis was established in the first three groups by bile duct ligation. Rats in the ZnPP and CoPP groups received once intraperitoneal injection of ZnPP and CoPP, respectively, 24 hours before sample collection.Expression of HO-1 mRNA in lung was detected by reverse-transcription polymerase chain reaction, while protein expression was determined by immunohistochemical analysis. Hematoxylin and eosin staining was performed to confirm the presence of liver cirrhosis and intrapulmonary vasodilation. Arterial blood gases, mean arterial pressure and portal vein pressure were also measured. Analysis of variance or Wilcoxon statistical methods were used to determine statistical significance.Results Compared with the sham group, the cirrhotic group demonstrated increased expression of pulmonary HO-1 mRNA and protein (P〈0.01). The level of arterial carboxyhemoglobin (COHb), alveolar-arterial oxygen gradient (A-aPO2),mean arterial pressure, portal vein pressure (P〈0.05, respectively), and intrapulmonary vasodilation were also significantly increased. Compared with the cirrhotic group, CoPP treatment increased pulmonary HO-1 mRNA and protein expression, the level of A-aPO2 (P 〈0.05 respectively), COHb (P 〈0.01), and intrapulmonary vasodilation, while ZnPP treatment decreased pulmonary HO-1 mRNA and protein expression, the level of COHb (P 〈0.05 respectively),and intrapulmonary vasodilation, without obvious alteration of mean arterial pressure and portal vein pressure.Conclusion Increased pulmonary HO-1 expression is an important contributor to the development of experimental HPS.</abstract><cop>China</cop><pub>Department of Gastroenterology, First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116001, China</pub><pmid>21518603</pmid><doi>10.3760/cma.j.issn.0366-6999.2011.06.021</doi><tpages>5</tpages></addata></record>
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subjects Animals
Enzyme Inhibitors - therapeutic use
Heme Oxygenase-1 - genetics
Heme Oxygenase-1 - metabolism
Hemodynamics
Immunohistochemistry
Liver Cirrhosis - enzymology
Liver Cirrhosis - genetics
Lung - drug effects
Lung - metabolism
Male
mRNA表达
Protoporphyrins - therapeutic use
Rats
Rats, Sprague-Dawley
Reverse Transcriptase Polymerase Chain Reaction
平均动脉压
本结构
肝硬化
肺功能
血红素氧化酶
逆转录聚合酶链反应
title Effects of heme oxygenase-1 on pulmonary function and structure in rats with liver cirrhosis
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