Pravastatin attenuates cardiac dysfunction induced by lysophosphatidylcholine in isolated rat hearts
Lysophosphatidylcholine (LPC), which accumulates in the ischemic myocardium, is responsible for mechanical and metabolic derangements of hearts, and also contributes to the development of ventricular arrhythmias. We examined the effects of pravastatin on the LPC-induced cardiac dysfunction in isolat...
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| Veröffentlicht in: | European journal of pharmacology 2010-08, Vol.640 (1), p.139-142 |
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| creator | Li, Libing Yao, Yuntai Wang, Hongye Ren, Yihong Ma, Lan Yan, Junlan Gao, Changqing |
| description | Lysophosphatidylcholine (LPC), which accumulates in the ischemic myocardium, is responsible for mechanical and metabolic derangements of hearts, and also contributes to the development of ventricular arrhythmias. We examined the effects of pravastatin on the LPC-induced cardiac dysfunction in isolated rat hearts. Rat hearts were randomly divided into four groups. The groups comprised a control group (
n
=
10), a group treated with LPC (5
μM) (
n
=
20), a group treated with pravastatin (400
ng/ml) (
n
=
10) and a group treated with both LPC and pravastatin (
n
=
20). Our data suggest that, pravastatin possesses some protective profiles against LPC, as manifested by better recovery of cardiac function (improvement in heart rate, left ventricular developed pressure, maximal and minimal first derivatives of left ventricular developed pressure, coronary flow and coronary resistance, less release of biomarkers of cardiac injury (lactate dehydrogenase, creatine kinase–MB and endothelin-1), and attenuation of ventricular arrhythmias (ventricular tachyarrhythmia and ventricular fibrillation). |
| doi_str_mv | 10.1016/j.ejphar.2010.04.052 |
| format | Article |
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n
=
10), a group treated with LPC (5
μM) (
n
=
20), a group treated with pravastatin (400
ng/ml) (
n
=
10) and a group treated with both LPC and pravastatin (
n
=
20). Our data suggest that, pravastatin possesses some protective profiles against LPC, as manifested by better recovery of cardiac function (improvement in heart rate, left ventricular developed pressure, maximal and minimal first derivatives of left ventricular developed pressure, coronary flow and coronary resistance, less release of biomarkers of cardiac injury (lactate dehydrogenase, creatine kinase–MB and endothelin-1), and attenuation of ventricular arrhythmias (ventricular tachyarrhythmia and ventricular fibrillation).</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/j.ejphar.2010.04.052</identifier><identifier>PMID: 20471973</identifier><identifier>CODEN: EJPHAZ</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Animals ; Biological and medical sciences ; Cardiac dysfunction ; Cardiac dysrhythmias ; Cardiology. Vascular system ; Creatine Kinase, MB Form - metabolism ; Endothelin-1 ; Endothelin-1 - metabolism ; Heart ; Heart - drug effects ; Heart - physiopathology ; Heart Ventricles - drug effects ; Heart Ventricles - metabolism ; Heart Ventricles - physiopathology ; Hemodynamics - drug effects ; L-Lactate Dehydrogenase - metabolism ; Lysophosphatidylcholine ; Lysophosphatidylcholines - pharmacology ; Male ; Medical sciences ; Pharmacology. Drug treatments ; Pravastatin ; Pravastatin - pharmacology ; Rats ; Rats, Sprague-Dawley ; Tachycardia - chemically induced ; Tachycardia - prevention & control ; Ventricular arrhythmias ; Ventricular Fibrillation - chemically induced ; Ventricular Fibrillation - prevention & control</subject><ispartof>European journal of pharmacology, 2010-08, Vol.640 (1), p.139-142</ispartof><rights>2010 Elsevier B.V.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright (c) 2010 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-89773674b8b50b28e04e79c7639721dae29540d68b888ff9b06b9bd20ce457733</citedby><cites>FETCH-LOGICAL-c391t-89773674b8b50b28e04e79c7639721dae29540d68b888ff9b06b9bd20ce457733</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ejphar.2010.04.052$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,782,786,3552,27931,27932,46002</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22980811$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20471973$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Libing</creatorcontrib><creatorcontrib>Yao, Yuntai</creatorcontrib><creatorcontrib>Wang, Hongye</creatorcontrib><creatorcontrib>Ren, Yihong</creatorcontrib><creatorcontrib>Ma, Lan</creatorcontrib><creatorcontrib>Yan, Junlan</creatorcontrib><creatorcontrib>Gao, Changqing</creatorcontrib><title>Pravastatin attenuates cardiac dysfunction induced by lysophosphatidylcholine in isolated rat hearts</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>Lysophosphatidylcholine (LPC), which accumulates in the ischemic myocardium, is responsible for mechanical and metabolic derangements of hearts, and also contributes to the development of ventricular arrhythmias. We examined the effects of pravastatin on the LPC-induced cardiac dysfunction in isolated rat hearts. Rat hearts were randomly divided into four groups. The groups comprised a control group (
n
=
10), a group treated with LPC (5
μM) (
n
=
20), a group treated with pravastatin (400
ng/ml) (
n
=
10) and a group treated with both LPC and pravastatin (
n
=
20). Our data suggest that, pravastatin possesses some protective profiles against LPC, as manifested by better recovery of cardiac function (improvement in heart rate, left ventricular developed pressure, maximal and minimal first derivatives of left ventricular developed pressure, coronary flow and coronary resistance, less release of biomarkers of cardiac injury (lactate dehydrogenase, creatine kinase–MB and endothelin-1), and attenuation of ventricular arrhythmias (ventricular tachyarrhythmia and ventricular fibrillation).</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiac dysfunction</subject><subject>Cardiac dysrhythmias</subject><subject>Cardiology. Vascular system</subject><subject>Creatine Kinase, MB Form - metabolism</subject><subject>Endothelin-1</subject><subject>Endothelin-1 - metabolism</subject><subject>Heart</subject><subject>Heart - drug effects</subject><subject>Heart - physiopathology</subject><subject>Heart Ventricles - drug effects</subject><subject>Heart Ventricles - metabolism</subject><subject>Heart Ventricles - physiopathology</subject><subject>Hemodynamics - drug effects</subject><subject>L-Lactate Dehydrogenase - metabolism</subject><subject>Lysophosphatidylcholine</subject><subject>Lysophosphatidylcholines - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Pharmacology. Drug treatments</subject><subject>Pravastatin</subject><subject>Pravastatin - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Tachycardia - chemically induced</subject><subject>Tachycardia - prevention & control</subject><subject>Ventricular arrhythmias</subject><subject>Ventricular Fibrillation - chemically induced</subject><subject>Ventricular Fibrillation - prevention & control</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE2LFDEQhoO4uOPqPxDpi-ypx0o63UkugizrByy4Bz2HfFQzGXo6Y5Je6H-_GWbUm6eC4nnfKh5C3lHYUqDDx_0W98edSVsGdQV8Cz17QTZUCtWCoOwl2QBQ3jKl1DV5nfMeAHrF-lfkmgEXVIluQ_xjMk8mF1PC3JhScF5Mwdw4k3wwrvFrHpfZlRDnJsx-cegbuzbTmuNxF3N9oAS_Tm4XpzBjRZqQ41QrfJNMaXZoUslvyNVopoxvL_OG_Ppy__PuW_vw4-v3u88PresULa1UQnSD4FbaHiyTCByFcmLolGDUG2Sq5-AHaaWU46gsDFZZz8Ah72u0uyG3595jir8XzEUfQnY4TWbGuGRdES76bqCV5GfSpZhzwlEfUziYtGoK-qRX7_VZrz7p1cB11Vtj7y8HFntA_zf0x2cFPlwAk52ZxmRmF_I_jikJkp7ufzpzWHU8BUw6u4BztRsSuqJ9DP__5Bkj9pvr</recordid><startdate>20100825</startdate><enddate>20100825</enddate><creator>Li, Libing</creator><creator>Yao, Yuntai</creator><creator>Wang, Hongye</creator><creator>Ren, Yihong</creator><creator>Ma, Lan</creator><creator>Yan, Junlan</creator><creator>Gao, Changqing</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><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></search><sort><creationdate>20100825</creationdate><title>Pravastatin attenuates cardiac dysfunction induced by lysophosphatidylcholine in isolated rat hearts</title><author>Li, Libing ; Yao, Yuntai ; Wang, Hongye ; Ren, Yihong ; Ma, Lan ; Yan, Junlan ; Gao, Changqing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-89773674b8b50b28e04e79c7639721dae29540d68b888ff9b06b9bd20ce457733</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiac dysfunction</topic><topic>Cardiac dysrhythmias</topic><topic>Cardiology. Vascular system</topic><topic>Creatine Kinase, MB Form - metabolism</topic><topic>Endothelin-1</topic><topic>Endothelin-1 - metabolism</topic><topic>Heart</topic><topic>Heart - drug effects</topic><topic>Heart - physiopathology</topic><topic>Heart Ventricles - drug effects</topic><topic>Heart Ventricles - metabolism</topic><topic>Heart Ventricles - physiopathology</topic><topic>Hemodynamics - drug effects</topic><topic>L-Lactate Dehydrogenase - metabolism</topic><topic>Lysophosphatidylcholine</topic><topic>Lysophosphatidylcholines - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Pharmacology. Drug treatments</topic><topic>Pravastatin</topic><topic>Pravastatin - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Tachycardia - chemically induced</topic><topic>Tachycardia - prevention & control</topic><topic>Ventricular arrhythmias</topic><topic>Ventricular Fibrillation - chemically induced</topic><topic>Ventricular Fibrillation - prevention & control</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Libing</creatorcontrib><creatorcontrib>Yao, Yuntai</creatorcontrib><creatorcontrib>Wang, Hongye</creatorcontrib><creatorcontrib>Ren, Yihong</creatorcontrib><creatorcontrib>Ma, Lan</creatorcontrib><creatorcontrib>Yan, Junlan</creatorcontrib><creatorcontrib>Gao, Changqing</creatorcontrib><collection>Pascal-Francis</collection><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>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Libing</au><au>Yao, Yuntai</au><au>Wang, Hongye</au><au>Ren, Yihong</au><au>Ma, Lan</au><au>Yan, Junlan</au><au>Gao, Changqing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pravastatin attenuates cardiac dysfunction induced by lysophosphatidylcholine in isolated rat hearts</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2010-08-25</date><risdate>2010</risdate><volume>640</volume><issue>1</issue><spage>139</spage><epage>142</epage><pages>139-142</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>Lysophosphatidylcholine (LPC), which accumulates in the ischemic myocardium, is responsible for mechanical and metabolic derangements of hearts, and also contributes to the development of ventricular arrhythmias. We examined the effects of pravastatin on the LPC-induced cardiac dysfunction in isolated rat hearts. Rat hearts were randomly divided into four groups. The groups comprised a control group (
n
=
10), a group treated with LPC (5
μM) (
n
=
20), a group treated with pravastatin (400
ng/ml) (
n
=
10) and a group treated with both LPC and pravastatin (
n
=
20). Our data suggest that, pravastatin possesses some protective profiles against LPC, as manifested by better recovery of cardiac function (improvement in heart rate, left ventricular developed pressure, maximal and minimal first derivatives of left ventricular developed pressure, coronary flow and coronary resistance, less release of biomarkers of cardiac injury (lactate dehydrogenase, creatine kinase–MB and endothelin-1), and attenuation of ventricular arrhythmias (ventricular tachyarrhythmia and ventricular fibrillation).</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>20471973</pmid><doi>10.1016/j.ejphar.2010.04.052</doi><tpages>4</tpages></addata></record> |
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| subjects | Animals Biological and medical sciences Cardiac dysfunction Cardiac dysrhythmias Cardiology. Vascular system Creatine Kinase, MB Form - metabolism Endothelin-1 Endothelin-1 - metabolism Heart Heart - drug effects Heart - physiopathology Heart Ventricles - drug effects Heart Ventricles - metabolism Heart Ventricles - physiopathology Hemodynamics - drug effects L-Lactate Dehydrogenase - metabolism Lysophosphatidylcholine Lysophosphatidylcholines - pharmacology Male Medical sciences Pharmacology. Drug treatments Pravastatin Pravastatin - pharmacology Rats Rats, Sprague-Dawley Tachycardia - chemically induced Tachycardia - prevention & control Ventricular arrhythmias Ventricular Fibrillation - chemically induced Ventricular Fibrillation - prevention & control |
| title | Pravastatin attenuates cardiac dysfunction induced by lysophosphatidylcholine in isolated rat hearts |
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