GW24-e3129 Protective Effects and Possible Mechanism on Left Ventricular Function after Delivery of Acidic Fibroblast Growth Factor to Diabetic Myocardium by Using Ultrasound-targeted Microbubble Destruction

Objectives To observe the protective effects of left ventricular function in diabetic cardiomyopathy rats after delivery of acidic fibroblast growth factor (aFGF) to myocardium by using ultrasound-targeted microbubble destruction (UTMD) and investigate the possible therapeutic mechanism. Methods Twe...

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Veröffentlicht in:Heart (British Cardiac Society) 2013-08, Vol.99 (Suppl 3), p.A271-A271
Hauptverfasser: Xinqiao, Tian, Ao, Ru, Yingzheng, Zhao, Jianmin, Li, Lei, Zheng, Keke, Jin, Chao, Zhang, Ge, Shuping
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container_issue Suppl 3
container_start_page A271
container_title Heart (British Cardiac Society)
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creator Xinqiao, Tian
Ao, Ru
Yingzheng, Zhao
Jianmin, Li
Lei, Zheng
Keke, Jin
Chao, Zhang
Ge, Shuping
description Objectives To observe the protective effects of left ventricular function in diabetic cardiomyopathy rats after delivery of acidic fibroblast growth factor (aFGF) to myocardium by using ultrasound-targeted microbubble destruction (UTMD) and investigate the possible therapeutic mechanism. Methods Twenty-four rats were induced to be DCM model by streptozotocin through intraperitoneal injecting and were randomly divided into the DCM group and the aFGF therapy group, and twelve normal rats were included as normal control group in the study. The aFGF therapy group animals were infused with SonoVue-aFGF mixed fluids through tail vein and simultaneous using UTMD. Four weeks after intervention, all rats underwent the cardiac catheter exam to obtaine the left ventricular contraction end pressure (LVESP), left ventricular end-diastolic pressure (LVEDP) and the maximal rate of pressure increase/decrease (± dp/dtmax). At last, myocardial tissue of all rats were stained with immunohistochemistry to quantify myocardial microvascular density, improved Masson staining of collagen to determination the myocardial collagen volume fraction (CVF), TUNEL method to detect the myocardial tissue apoptosis index (AI). Results Four weeks after intervention, the LVESP and LV ± dp/dtmax in the aFGF therapy group were significantly increased than in DCM group (P < 0.01), and the LVEDP in the aFGF therapy group were significantly lower than in the DCM group (P
doi_str_mv 10.1136/heartjnl-2013-304613.766
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Methods Twenty-four rats were induced to be DCM model by streptozotocin through intraperitoneal injecting and were randomly divided into the DCM group and the aFGF therapy group, and twelve normal rats were included as normal control group in the study. The aFGF therapy group animals were infused with SonoVue-aFGF mixed fluids through tail vein and simultaneous using UTMD. Four weeks after intervention, all rats underwent the cardiac catheter exam to obtaine the left ventricular contraction end pressure (LVESP), left ventricular end-diastolic pressure (LVEDP) and the maximal rate of pressure increase/decrease (± dp/dtmax). At last, myocardial tissue of all rats were stained with immunohistochemistry to quantify myocardial microvascular density, improved Masson staining of collagen to determination the myocardial collagen volume fraction (CVF), TUNEL method to detect the myocardial tissue apoptosis index (AI). Results Four weeks after intervention, the LVESP and LV ± dp/dtmax in the aFGF therapy group were significantly increased than in DCM group (P &lt; 0.01), and the LVEDP in the aFGF therapy group were significantly lower than in the DCM group (P &lt;0.01). The MVD in the aFGF therapy group were significantly increased than in DCM group (P &lt; 0.01), but the CVF and AI in the aFGF therapy group were significantly lower than in the DCM group (P &lt; 0.01). Conclusions Delivery of aFGF to diabetic myocardium by using UTMD could improve the left ventricular function and may be a new feasible therapeutic method for DCM.</description><identifier>ISSN: 1355-6037</identifier><identifier>EISSN: 1468-201X</identifier><identifier>DOI: 10.1136/heartjnl-2013-304613.766</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Cardiovascular Society</publisher><ispartof>Heart (British Cardiac Society), 2013-08, Vol.99 (Suppl 3), p.A271-A271</ispartof><rights>2013, Published by the bMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</rights><rights>Copyright: 2013 (c) 2013, Published by the bMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttp://heart.bmj.com/content/99/Suppl_3/A271.2.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttp://heart.bmj.com/content/99/Suppl_3/A271.2.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,314,778,782,3185,23554,27907,27908,77351,77382</link.rule.ids></links><search><creatorcontrib>Xinqiao, Tian</creatorcontrib><creatorcontrib>Ao, Ru</creatorcontrib><creatorcontrib>Yingzheng, Zhao</creatorcontrib><creatorcontrib>Jianmin, Li</creatorcontrib><creatorcontrib>Lei, Zheng</creatorcontrib><creatorcontrib>Keke, Jin</creatorcontrib><creatorcontrib>Chao, Zhang</creatorcontrib><creatorcontrib>Ge, Shuping</creatorcontrib><title>GW24-e3129 Protective Effects and Possible Mechanism on Left Ventricular Function after Delivery of Acidic Fibroblast Growth Factor to Diabetic Myocardium by Using Ultrasound-targeted Microbubble Destruction</title><title>Heart (British Cardiac Society)</title><addtitle>Heart</addtitle><description>Objectives To observe the protective effects of left ventricular function in diabetic cardiomyopathy rats after delivery of acidic fibroblast growth factor (aFGF) to myocardium by using ultrasound-targeted microbubble destruction (UTMD) and investigate the possible therapeutic mechanism. Methods Twenty-four rats were induced to be DCM model by streptozotocin through intraperitoneal injecting and were randomly divided into the DCM group and the aFGF therapy group, and twelve normal rats were included as normal control group in the study. The aFGF therapy group animals were infused with SonoVue-aFGF mixed fluids through tail vein and simultaneous using UTMD. Four weeks after intervention, all rats underwent the cardiac catheter exam to obtaine the left ventricular contraction end pressure (LVESP), left ventricular end-diastolic pressure (LVEDP) and the maximal rate of pressure increase/decrease (± dp/dtmax). At last, myocardial tissue of all rats were stained with immunohistochemistry to quantify myocardial microvascular density, improved Masson staining of collagen to determination the myocardial collagen volume fraction (CVF), TUNEL method to detect the myocardial tissue apoptosis index (AI). Results Four weeks after intervention, the LVESP and LV ± dp/dtmax in the aFGF therapy group were significantly increased than in DCM group (P &lt; 0.01), and the LVEDP in the aFGF therapy group were significantly lower than in the DCM group (P &lt;0.01). The MVD in the aFGF therapy group were significantly increased than in DCM group (P &lt; 0.01), but the CVF and AI in the aFGF therapy group were significantly lower than in the DCM group (P &lt; 0.01). Conclusions Delivery of aFGF to diabetic myocardium by using UTMD could improve the left ventricular function and may be a new feasible therapeutic method for DCM.</description><issn>1355-6037</issn><issn>1468-201X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNUc2O0zAQjhBILAvvMBLnLHacOMlx1W4Kol0WiS7crHEy2bqk8WI7QG9ceEBegSfBJcCZ03ya-X5G-pIEOLvgXMgXO0IX9uOQZoyLVLBccnFRSvkgOeO5rE7rDw8jFkWRSibKx8kT7_eMsbyu5FnyY_U-y1MSPKt_fvt-42ygNpjPBFd9H5EHHDu4sd4bPRBsqN3haPwB7Ahr6gPc0hicaacBHTTTGLXxgn0gB0saopE7gu3hsjWdaaEx2lk9oA-wcvZL2EGDbbAOgoWlQU0hkjZH26LrzHQAfYStN-MdbIfg0Ntp7NKA7o4CdbAxbTSb9OmxJfngpt_pT5NHPQ6env2Z58m2uXq3eJmu36xeLS7XqeZFLVOdZTnVJPKOiy6PuJeEVV2RzCvEru9boQtZZpmsO41YM2IFxxLrMpNFLjtxnjyffe-d_TTFfLW3kxtjpOJlxUqR8UpGVjWz4q_eO-rVvTMHdEfFmToVqP4WqE4FqrlAFQuM0nSWGh_o6z8duo9KlqIs1PXtQq1Wb5evi-tKNZEvZr4-7P8_5Rdoi7Vu</recordid><startdate>201308</startdate><enddate>201308</enddate><creator>Xinqiao, Tian</creator><creator>Ao, Ru</creator><creator>Yingzheng, Zhao</creator><creator>Jianmin, Li</creator><creator>Lei, Zheng</creator><creator>Keke, Jin</creator><creator>Chao, Zhang</creator><creator>Ge, Shuping</creator><general>BMJ Publishing Group Ltd and British Cardiovascular Society</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope></search><sort><creationdate>201308</creationdate><title>GW24-e3129 Protective Effects and Possible Mechanism on Left Ventricular Function after Delivery of Acidic Fibroblast Growth Factor to Diabetic Myocardium by Using Ultrasound-targeted Microbubble Destruction</title><author>Xinqiao, Tian ; Ao, Ru ; Yingzheng, Zhao ; Jianmin, Li ; Lei, Zheng ; Keke, Jin ; Chao, Zhang ; Ge, Shuping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b1596-b224e9e34d13d424ef6ea898e648aadffc3b5672269dbaa90e051a7a9726546d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xinqiao, Tian</creatorcontrib><creatorcontrib>Ao, Ru</creatorcontrib><creatorcontrib>Yingzheng, Zhao</creatorcontrib><creatorcontrib>Jianmin, Li</creatorcontrib><creatorcontrib>Lei, Zheng</creatorcontrib><creatorcontrib>Keke, Jin</creatorcontrib><creatorcontrib>Chao, Zhang</creatorcontrib><creatorcontrib>Ge, Shuping</creatorcontrib><collection>Istex</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><jtitle>Heart (British Cardiac Society)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xinqiao, Tian</au><au>Ao, Ru</au><au>Yingzheng, Zhao</au><au>Jianmin, Li</au><au>Lei, Zheng</au><au>Keke, Jin</au><au>Chao, Zhang</au><au>Ge, Shuping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>GW24-e3129 Protective Effects and Possible Mechanism on Left Ventricular Function after Delivery of Acidic Fibroblast Growth Factor to Diabetic Myocardium by Using Ultrasound-targeted Microbubble Destruction</atitle><jtitle>Heart (British Cardiac Society)</jtitle><addtitle>Heart</addtitle><date>2013-08</date><risdate>2013</risdate><volume>99</volume><issue>Suppl 3</issue><spage>A271</spage><epage>A271</epage><pages>A271-A271</pages><issn>1355-6037</issn><eissn>1468-201X</eissn><abstract>Objectives To observe the protective effects of left ventricular function in diabetic cardiomyopathy rats after delivery of acidic fibroblast growth factor (aFGF) to myocardium by using ultrasound-targeted microbubble destruction (UTMD) and investigate the possible therapeutic mechanism. Methods Twenty-four rats were induced to be DCM model by streptozotocin through intraperitoneal injecting and were randomly divided into the DCM group and the aFGF therapy group, and twelve normal rats were included as normal control group in the study. The aFGF therapy group animals were infused with SonoVue-aFGF mixed fluids through tail vein and simultaneous using UTMD. Four weeks after intervention, all rats underwent the cardiac catheter exam to obtaine the left ventricular contraction end pressure (LVESP), left ventricular end-diastolic pressure (LVEDP) and the maximal rate of pressure increase/decrease (± dp/dtmax). At last, myocardial tissue of all rats were stained with immunohistochemistry to quantify myocardial microvascular density, improved Masson staining of collagen to determination the myocardial collagen volume fraction (CVF), TUNEL method to detect the myocardial tissue apoptosis index (AI). Results Four weeks after intervention, the LVESP and LV ± dp/dtmax in the aFGF therapy group were significantly increased than in DCM group (P &lt; 0.01), and the LVEDP in the aFGF therapy group were significantly lower than in the DCM group (P &lt;0.01). The MVD in the aFGF therapy group were significantly increased than in DCM group (P &lt; 0.01), but the CVF and AI in the aFGF therapy group were significantly lower than in the DCM group (P &lt; 0.01). Conclusions Delivery of aFGF to diabetic myocardium by using UTMD could improve the left ventricular function and may be a new feasible therapeutic method for DCM.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Cardiovascular Society</pub><doi>10.1136/heartjnl-2013-304613.766</doi></addata></record>
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title GW24-e3129 Protective Effects and Possible Mechanism on Left Ventricular Function after Delivery of Acidic Fibroblast Growth Factor to Diabetic Myocardium by Using Ultrasound-targeted Microbubble Destruction
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