Propofol improves cardiac functional recovery after ischemia-reperfusion by upregulating nitric oxide synthase activity in the isolated rat hearts

Background There are few studies to assess whether propofol attenuates myocardial ischemia-reperfusion injury via a mechanism related to nitric oxide (NO) route, so we designed this randomized blinded experiment to observe the changes of NO contents, nitric oxide synthase (NOS) activity, NOS content...

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Veröffentlicht in:Chinese medical journal 2009-12, Vol.122 (24), p.3048-3054
Hauptverfasser: Sun, Hai-Yan, Xue, Fu-Shan, Xu, Ya-Chao, Li, Cheng-Wen, Xiong, Jun, Liao, Xu, Zhang, Yan-Ming
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container_end_page 3054
container_issue 24
container_start_page 3048
container_title Chinese medical journal
container_volume 122
creator Sun, Hai-Yan
Xue, Fu-Shan
Xu, Ya-Chao
Li, Cheng-Wen
Xiong, Jun
Liao, Xu
Zhang, Yan-Ming
description Background There are few studies to assess whether propofol attenuates myocardial ischemia-reperfusion injury via a mechanism related to nitric oxide (NO) route, so we designed this randomized blinded experiment to observe the changes of NO contents, nitric oxide synthase (NOS) activity, NOS contents in the myocardium, and cardiac function in ischemic reperfused isolated rat hearts, and to assess the relation between myocardial NO system and cardioprotection of propofol. Methods The hearts of 30 Sprague-Dawley male rats were removed, mounted on a Langendorff apparatus, and randomly assigned to one of three groups (n=10 each group) to be treated with the following treatments in a blinded manner: Group 1, control group, after perfusion with pure Krebs Henseleit bicarbonate (K-HBB) buffer solution for 15 minutes, hearts were subjected to 20 minutes global ischemia followed by 60 minutes reperfusion with pure K-HBB buffer; Group 2, after perfusion with K-HBB buffer solution containing propofol (10 ug/ml) for 15 minutes, the hearts underwent 20 minutes global ischemia followed by 60 minutes reperfusion with the same K-HBB buffer solution; Group 3, after perfusion with K-HBB buffer solution containing propofol (10ug/ml) and L-NAME (100 umol/L) for 15 minutes, the hearts underwent 20 minutes global ischemia followed by 60 minutes reperfusion with the same K-HBB buffer solution. The cardiac function was continuously monitored throughout the experiment. The coronary flow was also measured. An ISO-NO electrode was placed into the right atrium close to the coronary sinus to continuously measure NO concentration in the coronary effluent. The tissue samples from apex of hearts in Groups 1 and 2 were obtained to measure the NOS activity by spectrophotometry and the NOS contents by immunohistochemistry, respectively. Results The cardiac function was significantly inhibited after ischemia and then gradually improved with reperfusion in all three groups. As compared with Group 1, the cardiac function variables and coronary flow at all the observed points were significantly improved in Group 2. The cardiac function variables and coronary flow were better in Group 3 than in Group 1, but were inferior in Group 3 than in Group 2. Both NO contents and NOS activity in the myocardium were significantly higher in Group 2 than in Group 1. However, NOS contents in the myocardium did not significantly differ between Groups 1 and 2. Conclusions In isolated rat hearts, propofol can imp
doi_str_mv 10.3760/cma.j.issn.0366-6999.2009.24.026
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Methods The hearts of 30 Sprague-Dawley male rats were removed, mounted on a Langendorff apparatus, and randomly assigned to one of three groups (n=10 each group) to be treated with the following treatments in a blinded manner: Group 1, control group, after perfusion with pure Krebs Henseleit bicarbonate (K-HBB) buffer solution for 15 minutes, hearts were subjected to 20 minutes global ischemia followed by 60 minutes reperfusion with pure K-HBB buffer; Group 2, after perfusion with K-HBB buffer solution containing propofol (10 ug/ml) for 15 minutes, the hearts underwent 20 minutes global ischemia followed by 60 minutes reperfusion with the same K-HBB buffer solution; Group 3, after perfusion with K-HBB buffer solution containing propofol (10ug/ml) and L-NAME (100 umol/L) for 15 minutes, the hearts underwent 20 minutes global ischemia followed by 60 minutes reperfusion with the same K-HBB buffer solution. The cardiac function was continuously monitored throughout the experiment. The coronary flow was also measured. An ISO-NO electrode was placed into the right atrium close to the coronary sinus to continuously measure NO concentration in the coronary effluent. The tissue samples from apex of hearts in Groups 1 and 2 were obtained to measure the NOS activity by spectrophotometry and the NOS contents by immunohistochemistry, respectively. Results The cardiac function was significantly inhibited after ischemia and then gradually improved with reperfusion in all three groups. As compared with Group 1, the cardiac function variables and coronary flow at all the observed points were significantly improved in Group 2. The cardiac function variables and coronary flow were better in Group 3 than in Group 1, but were inferior in Group 3 than in Group 2. Both NO contents and NOS activity in the myocardium were significantly higher in Group 2 than in Group 1. However, NOS contents in the myocardium did not significantly differ between Groups 1 and 2. Conclusions In isolated rat hearts, propofol can improve cardiac functional recovery after ischemia-reperfusion by upregulating NOS activity in the myocardium. The NO system may play an important role in the preservation of myocardial ischemia-reperfusion injury produced by propofol.</description><identifier>ISSN: 0366-6999</identifier><identifier>EISSN: 2542-5641</identifier><identifier>DOI: 10.3760/cma.j.issn.0366-6999.2009.24.026</identifier><identifier>PMID: 20137500</identifier><language>eng</language><publisher>China: Department of Anesthesiology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China%Department of Anesthesiology, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing 100144, China</publisher><subject>Animals ; Coronary Circulation - drug effects ; Enzyme Activation - drug effects ; Heart - drug effects ; Heart Function Tests ; Hypnotics and Sedatives - pharmacology ; Hypnotics and Sedatives - therapeutic use ; Immunohistochemistry ; In Vitro Techniques ; Male ; Myocardial Reperfusion Injury - drug therapy ; Myocardial Reperfusion Injury - enzymology ; Myocardium - enzymology ; Nitric Oxide Synthase - metabolism ; Propofol - pharmacology ; Propofol - therapeutic use ; Rats ; Rats, Sprague-Dawley ; SD大鼠 ; 一氧化氮合酶 ; 功能恢复 ; 异丙酚 ; 心肌缺血再灌注 ; 离体心脏 ; 缓冲溶液 ; 酶活性</subject><ispartof>Chinese medical journal, 2009-12, Vol.122 (24), p.3048-3054</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>$$Uhttp://image.cqvip.com/vip1000/qk/85656X/85656X.jpg</thumbnail><link.rule.ids>315,781,785,865,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20137500$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, Hai-Yan</creatorcontrib><creatorcontrib>Xue, Fu-Shan</creatorcontrib><creatorcontrib>Xu, Ya-Chao</creatorcontrib><creatorcontrib>Li, Cheng-Wen</creatorcontrib><creatorcontrib>Xiong, Jun</creatorcontrib><creatorcontrib>Liao, Xu</creatorcontrib><creatorcontrib>Zhang, Yan-Ming</creatorcontrib><title>Propofol improves cardiac functional recovery after ischemia-reperfusion by upregulating nitric oxide synthase activity in the isolated rat hearts</title><title>Chinese medical journal</title><addtitle>Chinese Medical Journal</addtitle><description>Background There are few studies to assess whether propofol attenuates myocardial ischemia-reperfusion injury via a mechanism related to nitric oxide (NO) route, so we designed this randomized blinded experiment to observe the changes of NO contents, nitric oxide synthase (NOS) activity, NOS contents in the myocardium, and cardiac function in ischemic reperfused isolated rat hearts, and to assess the relation between myocardial NO system and cardioprotection of propofol. Methods The hearts of 30 Sprague-Dawley male rats were removed, mounted on a Langendorff apparatus, and randomly assigned to one of three groups (n=10 each group) to be treated with the following treatments in a blinded manner: Group 1, control group, after perfusion with pure Krebs Henseleit bicarbonate (K-HBB) buffer solution for 15 minutes, hearts were subjected to 20 minutes global ischemia followed by 60 minutes reperfusion with pure K-HBB buffer; Group 2, after perfusion with K-HBB buffer solution containing propofol (10 ug/ml) for 15 minutes, the hearts underwent 20 minutes global ischemia followed by 60 minutes reperfusion with the same K-HBB buffer solution; Group 3, after perfusion with K-HBB buffer solution containing propofol (10ug/ml) and L-NAME (100 umol/L) for 15 minutes, the hearts underwent 20 minutes global ischemia followed by 60 minutes reperfusion with the same K-HBB buffer solution. The cardiac function was continuously monitored throughout the experiment. The coronary flow was also measured. An ISO-NO electrode was placed into the right atrium close to the coronary sinus to continuously measure NO concentration in the coronary effluent. The tissue samples from apex of hearts in Groups 1 and 2 were obtained to measure the NOS activity by spectrophotometry and the NOS contents by immunohistochemistry, respectively. Results The cardiac function was significantly inhibited after ischemia and then gradually improved with reperfusion in all three groups. As compared with Group 1, the cardiac function variables and coronary flow at all the observed points were significantly improved in Group 2. The cardiac function variables and coronary flow were better in Group 3 than in Group 1, but were inferior in Group 3 than in Group 2. Both NO contents and NOS activity in the myocardium were significantly higher in Group 2 than in Group 1. However, NOS contents in the myocardium did not significantly differ between Groups 1 and 2. Conclusions In isolated rat hearts, propofol can improve cardiac functional recovery after ischemia-reperfusion by upregulating NOS activity in the myocardium. The NO system may play an important role in the preservation of myocardial ischemia-reperfusion injury produced by propofol.</description><subject>Animals</subject><subject>Coronary Circulation - drug effects</subject><subject>Enzyme Activation - drug effects</subject><subject>Heart - drug effects</subject><subject>Heart Function Tests</subject><subject>Hypnotics and Sedatives - pharmacology</subject><subject>Hypnotics and Sedatives - therapeutic use</subject><subject>Immunohistochemistry</subject><subject>In Vitro Techniques</subject><subject>Male</subject><subject>Myocardial Reperfusion Injury - drug therapy</subject><subject>Myocardial Reperfusion Injury - enzymology</subject><subject>Myocardium - enzymology</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Propofol - pharmacology</subject><subject>Propofol - therapeutic use</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>SD大鼠</subject><subject>一氧化氮合酶</subject><subject>功能恢复</subject><subject>异丙酚</subject><subject>心肌缺血再灌注</subject><subject>离体心脏</subject><subject>缓冲溶液</subject><subject>酶活性</subject><issn>0366-6999</issn><issn>2542-5641</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo90Mtu1TAQgGELgehp4RWQxQK6SfAlcZIlqrhJlWAB62jijE98SOzUdgrhMXhijE5h41n400jzE3LNWSkbxd7oBcpTaWN0JZNKFarrulIwlp-qZEI9IgdRV6KoVcUfk8N_c0EuYzwxJuq6UU_JhWBcNjVjB_L7S_CrN36mdlmDv8dINYTRgqZmczpZ72CmAXX-CjsFkzBQG_WEi4Ui4IrBbDErOux0WwMetxmSdUfqbApWU__Tjkjj7tIEESnklfc27dQ6mibMq3z2ONIAiU4IIcVn5ImBOeLzh3lFvr1_9_XmY3H7-cOnm7e3hRaqTYXSaKA1teZmaKEx7ci0GcdKKd5UssKhEp1Qqh0YGKmwy0NwzptWNhoapuQVeXXe-wOcAXfsT34L-drY_5r0cvqbVVQ5aoavzzAHutswpn7JBXCewaHfYt9I2UnWqirLFw9yGxYc-zXYBcLe_-udwcsz0JN3x7vcqR9Afzd2xl6KWimpuPwDW4eWKg</recordid><startdate>20091220</startdate><enddate>20091220</enddate><creator>Sun, Hai-Yan</creator><creator>Xue, Fu-Shan</creator><creator>Xu, Ya-Chao</creator><creator>Li, Cheng-Wen</creator><creator>Xiong, Jun</creator><creator>Liao, Xu</creator><creator>Zhang, Yan-Ming</creator><general>Department of Anesthesiology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China%Department of Anesthesiology, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing 100144, China</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W94</scope><scope>WU4</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>20091220</creationdate><title>Propofol improves cardiac functional recovery after ischemia-reperfusion by upregulating nitric oxide synthase activity in the isolated rat hearts</title><author>Sun, Hai-Yan ; Xue, Fu-Shan ; Xu, Ya-Chao ; Li, Cheng-Wen ; Xiong, Jun ; Liao, Xu ; Zhang, Yan-Ming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c268t-6cefa8f5c1fb8a7f8d0cfdd46617434eb4292668b0af36e90af21117837ca7063</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Coronary Circulation - drug effects</topic><topic>Enzyme Activation - drug effects</topic><topic>Heart - drug effects</topic><topic>Heart Function Tests</topic><topic>Hypnotics and Sedatives - pharmacology</topic><topic>Hypnotics and Sedatives - therapeutic use</topic><topic>Immunohistochemistry</topic><topic>In Vitro Techniques</topic><topic>Male</topic><topic>Myocardial Reperfusion Injury - drug therapy</topic><topic>Myocardial Reperfusion Injury - enzymology</topic><topic>Myocardium - enzymology</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Propofol - pharmacology</topic><topic>Propofol - therapeutic use</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>SD大鼠</topic><topic>一氧化氮合酶</topic><topic>功能恢复</topic><topic>异丙酚</topic><topic>心肌缺血再灌注</topic><topic>离体心脏</topic><topic>缓冲溶液</topic><topic>酶活性</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sun, Hai-Yan</creatorcontrib><creatorcontrib>Xue, Fu-Shan</creatorcontrib><creatorcontrib>Xu, Ya-Chao</creatorcontrib><creatorcontrib>Li, Cheng-Wen</creatorcontrib><creatorcontrib>Xiong, Jun</creatorcontrib><creatorcontrib>Liao, Xu</creatorcontrib><creatorcontrib>Zhang, Yan-Ming</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-自然科学</collection><collection>中文科技期刊数据库-自然科学-生物科学</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>Sun, Hai-Yan</au><au>Xue, Fu-Shan</au><au>Xu, Ya-Chao</au><au>Li, Cheng-Wen</au><au>Xiong, Jun</au><au>Liao, Xu</au><au>Zhang, Yan-Ming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Propofol improves cardiac functional recovery after ischemia-reperfusion by upregulating nitric oxide synthase activity in the isolated rat hearts</atitle><jtitle>Chinese medical journal</jtitle><addtitle>Chinese Medical Journal</addtitle><date>2009-12-20</date><risdate>2009</risdate><volume>122</volume><issue>24</issue><spage>3048</spage><epage>3054</epage><pages>3048-3054</pages><issn>0366-6999</issn><eissn>2542-5641</eissn><abstract>Background There are few studies to assess whether propofol attenuates myocardial ischemia-reperfusion injury via a mechanism related to nitric oxide (NO) route, so we designed this randomized blinded experiment to observe the changes of NO contents, nitric oxide synthase (NOS) activity, NOS contents in the myocardium, and cardiac function in ischemic reperfused isolated rat hearts, and to assess the relation between myocardial NO system and cardioprotection of propofol. Methods The hearts of 30 Sprague-Dawley male rats were removed, mounted on a Langendorff apparatus, and randomly assigned to one of three groups (n=10 each group) to be treated with the following treatments in a blinded manner: Group 1, control group, after perfusion with pure Krebs Henseleit bicarbonate (K-HBB) buffer solution for 15 minutes, hearts were subjected to 20 minutes global ischemia followed by 60 minutes reperfusion with pure K-HBB buffer; Group 2, after perfusion with K-HBB buffer solution containing propofol (10 ug/ml) for 15 minutes, the hearts underwent 20 minutes global ischemia followed by 60 minutes reperfusion with the same K-HBB buffer solution; Group 3, after perfusion with K-HBB buffer solution containing propofol (10ug/ml) and L-NAME (100 umol/L) for 15 minutes, the hearts underwent 20 minutes global ischemia followed by 60 minutes reperfusion with the same K-HBB buffer solution. The cardiac function was continuously monitored throughout the experiment. The coronary flow was also measured. An ISO-NO electrode was placed into the right atrium close to the coronary sinus to continuously measure NO concentration in the coronary effluent. The tissue samples from apex of hearts in Groups 1 and 2 were obtained to measure the NOS activity by spectrophotometry and the NOS contents by immunohistochemistry, respectively. Results The cardiac function was significantly inhibited after ischemia and then gradually improved with reperfusion in all three groups. As compared with Group 1, the cardiac function variables and coronary flow at all the observed points were significantly improved in Group 2. The cardiac function variables and coronary flow were better in Group 3 than in Group 1, but were inferior in Group 3 than in Group 2. Both NO contents and NOS activity in the myocardium were significantly higher in Group 2 than in Group 1. However, NOS contents in the myocardium did not significantly differ between Groups 1 and 2. Conclusions In isolated rat hearts, propofol can improve cardiac functional recovery after ischemia-reperfusion by upregulating NOS activity in the myocardium. The NO system may play an important role in the preservation of myocardial ischemia-reperfusion injury produced by propofol.</abstract><cop>China</cop><pub>Department of Anesthesiology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China%Department of Anesthesiology, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing 100144, China</pub><pmid>20137500</pmid><doi>10.3760/cma.j.issn.0366-6999.2009.24.026</doi><tpages>7</tpages></addata></record>
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subjects Animals
Coronary Circulation - drug effects
Enzyme Activation - drug effects
Heart - drug effects
Heart Function Tests
Hypnotics and Sedatives - pharmacology
Hypnotics and Sedatives - therapeutic use
Immunohistochemistry
In Vitro Techniques
Male
Myocardial Reperfusion Injury - drug therapy
Myocardial Reperfusion Injury - enzymology
Myocardium - enzymology
Nitric Oxide Synthase - metabolism
Propofol - pharmacology
Propofol - therapeutic use
Rats
Rats, Sprague-Dawley
SD大鼠
一氧化氮合酶
功能恢复
异丙酚
心肌缺血再灌注
离体心脏
缓冲溶液
酶活性
title Propofol improves cardiac functional recovery after ischemia-reperfusion by upregulating nitric oxide synthase activity in the isolated rat hearts
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