Amrinone reduces ischaemia–reperfusion injury in rat heart
We investigated the effects of amrinone on ischaemia-induced changes in myocardial function in isolated rat hearts. Isolated hearts from male Sprague–Dawley rats (150–275 g) were perfused with physiological salt solution at a constant flow rate. The effects of amrinone (30 μM) on left ventricular en...
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| Veröffentlicht in: | European journal of pharmacology 2000-08, Vol.402 (3), p.255-262 |
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| creator | Rechtman, Mary P Van der Zypp, Andrea Majewski, Henryk |
| description | We investigated the effects of amrinone on ischaemia-induced changes in myocardial function in isolated rat hearts. Isolated hearts from male Sprague–Dawley rats (150–275 g) were perfused with physiological salt solution at a constant flow rate. The effects of amrinone (30 μM) on left ventricular end diastolic pressure, positive and negative d
P/d
t, heart rate and coronary perfusion pressure were observed following global ischaemia and reperfusion. In normal hearts, amrinone had no effect on myocardial contractility, heart rate, coronary perfusion pressure or left ventricular end diastolic pressure. Ischaemia–reperfusion caused an increase in coronary perfusion pressure, left ventricular end diastolic pressure and creatine kinase outflow and amrinone (present from before ischaemia) decreased the rise in all of these parameters. However, when amrinone was added only after the ischaemia, it had no effect on coronary perfusion pressure or left ventricular end diastolic pressure. Thus, the effect on coronary perfusion pressure must be due to actions during the ischaemia phase. We suggest that amrinone has pharmacological properties which may be useful in reducing ischaemia–reperfusion injury. We speculate that this involves altering ischaemia-induced changes in intracellular Ca
2+ in the myocytes. |
| doi_str_mv | 10.1016/S0014-2999(00)00443-X |
| format | Article |
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P/d
t, heart rate and coronary perfusion pressure were observed following global ischaemia and reperfusion. In normal hearts, amrinone had no effect on myocardial contractility, heart rate, coronary perfusion pressure or left ventricular end diastolic pressure. Ischaemia–reperfusion caused an increase in coronary perfusion pressure, left ventricular end diastolic pressure and creatine kinase outflow and amrinone (present from before ischaemia) decreased the rise in all of these parameters. However, when amrinone was added only after the ischaemia, it had no effect on coronary perfusion pressure or left ventricular end diastolic pressure. Thus, the effect on coronary perfusion pressure must be due to actions during the ischaemia phase. We suggest that amrinone has pharmacological properties which may be useful in reducing ischaemia–reperfusion injury. We speculate that this involves altering ischaemia-induced changes in intracellular Ca
2+ in the myocytes.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/S0014-2999(00)00443-X</identifier><identifier>PMID: 10958893</identifier><identifier>CODEN: EJPHAZ</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>1-Methyl-3-isobutylxanthine - pharmacology ; 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester - pharmacology ; Amrinone ; Amrinone - pharmacology ; Animals ; Biological and medical sciences ; Cardiotonic Agents - pharmacology ; Cardiovascular system ; Creatine Kinase - metabolism ; Ischaemia ; L-Lactate Dehydrogenase - metabolism ; Male ; Medical sciences ; Milrinone - pharmacology ; Miscellaneous ; Myocardial Reperfusion Injury - drug therapy ; Myocardial Reperfusion Injury - pathology ; Myocardium - pathology ; Pharmacology. Drug treatments ; Phosphodiesterase Inhibitors - pharmacology ; Rat ; Rats ; Rats, Sprague-Dawley ; Reperfusion injury ; Vasodilation - drug effects</subject><ispartof>European journal of pharmacology, 2000-08, Vol.402 (3), p.255-262</ispartof><rights>2000 Elsevier Science B.V.</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-505d9d2bf1e360c62c1812859c3d668285b5a2a615b1cfb02c93edd056876c373</citedby><cites>FETCH-LOGICAL-c390t-505d9d2bf1e360c62c1812859c3d668285b5a2a615b1cfb02c93edd056876c373</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S001429990000443X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1473367$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10958893$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rechtman, Mary P</creatorcontrib><creatorcontrib>Van der Zypp, Andrea</creatorcontrib><creatorcontrib>Majewski, Henryk</creatorcontrib><title>Amrinone reduces ischaemia–reperfusion injury in rat heart</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>We investigated the effects of amrinone on ischaemia-induced changes in myocardial function in isolated rat hearts. Isolated hearts from male Sprague–Dawley rats (150–275 g) were perfused with physiological salt solution at a constant flow rate. The effects of amrinone (30 μM) on left ventricular end diastolic pressure, positive and negative d
P/d
t, heart rate and coronary perfusion pressure were observed following global ischaemia and reperfusion. In normal hearts, amrinone had no effect on myocardial contractility, heart rate, coronary perfusion pressure or left ventricular end diastolic pressure. Ischaemia–reperfusion caused an increase in coronary perfusion pressure, left ventricular end diastolic pressure and creatine kinase outflow and amrinone (present from before ischaemia) decreased the rise in all of these parameters. However, when amrinone was added only after the ischaemia, it had no effect on coronary perfusion pressure or left ventricular end diastolic pressure. Thus, the effect on coronary perfusion pressure must be due to actions during the ischaemia phase. We suggest that amrinone has pharmacological properties which may be useful in reducing ischaemia–reperfusion injury. We speculate that this involves altering ischaemia-induced changes in intracellular Ca
2+ in the myocytes.</description><subject>1-Methyl-3-isobutylxanthine - pharmacology</subject><subject>3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester - pharmacology</subject><subject>Amrinone</subject><subject>Amrinone - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Cardiovascular system</subject><subject>Creatine Kinase - metabolism</subject><subject>Ischaemia</subject><subject>L-Lactate Dehydrogenase - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Milrinone - pharmacology</subject><subject>Miscellaneous</subject><subject>Myocardial Reperfusion Injury - drug therapy</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocardium - pathology</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphodiesterase Inhibitors - pharmacology</subject><subject>Rat</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion injury</subject><subject>Vasodilation - drug effects</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM9KxDAQh4Mouq4-gtKDiB6qk6RJGxBExH-w4EEFbyFNphjZtmvSCt58B9_QJ7HrLurN08zh-838-AjZoXBEgcrjOwCapUwpdQBwCJBlPH1cISNa5CqFnLJVMvpBNshmjM8AIBQT62SDghJFofiInJzVwTdtg0lA11uMiY_2yWDtzef7R8AZhqqPvm0S3zz34W0YSTBd8oQmdFtkrTLTiNvLOSYPlxf359fp5Pbq5vxsklquoEsFCKccKyuKXIKVzNKCskIoy52UxbCVwjAjqSiprUpgVnF0DoQscml5zsdkf3F3FtqXHmOn66ElTqemwbaPOmeMygzoAIoFaEMbY8BKz4KvTXjTFPRcm_7WpudONID-1qYfh9zu8kFf1uj-pBaeBmBvCZhozbQKprE-_nJZzrmcFz1dYDjYePUYdLQeG4vOB7Sddq3_p8kXbISJpA</recordid><startdate>20000825</startdate><enddate>20000825</enddate><creator>Rechtman, Mary P</creator><creator>Van der Zypp, Andrea</creator><creator>Majewski, Henryk</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>20000825</creationdate><title>Amrinone reduces ischaemia–reperfusion injury in rat heart</title><author>Rechtman, Mary P ; Van der Zypp, Andrea ; Majewski, Henryk</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-505d9d2bf1e360c62c1812859c3d668285b5a2a615b1cfb02c93edd056876c373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>1-Methyl-3-isobutylxanthine - pharmacology</topic><topic>3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester - pharmacology</topic><topic>Amrinone</topic><topic>Amrinone - pharmacology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Cardiovascular system</topic><topic>Creatine Kinase - metabolism</topic><topic>Ischaemia</topic><topic>L-Lactate Dehydrogenase - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Milrinone - pharmacology</topic><topic>Miscellaneous</topic><topic>Myocardial Reperfusion Injury - drug therapy</topic><topic>Myocardial Reperfusion Injury - pathology</topic><topic>Myocardium - pathology</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphodiesterase Inhibitors - pharmacology</topic><topic>Rat</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion injury</topic><topic>Vasodilation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rechtman, Mary P</creatorcontrib><creatorcontrib>Van der Zypp, Andrea</creatorcontrib><creatorcontrib>Majewski, Henryk</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>Rechtman, Mary P</au><au>Van der Zypp, Andrea</au><au>Majewski, Henryk</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Amrinone reduces ischaemia–reperfusion injury in rat heart</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2000-08-25</date><risdate>2000</risdate><volume>402</volume><issue>3</issue><spage>255</spage><epage>262</epage><pages>255-262</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>We investigated the effects of amrinone on ischaemia-induced changes in myocardial function in isolated rat hearts. Isolated hearts from male Sprague–Dawley rats (150–275 g) were perfused with physiological salt solution at a constant flow rate. The effects of amrinone (30 μM) on left ventricular end diastolic pressure, positive and negative d
P/d
t, heart rate and coronary perfusion pressure were observed following global ischaemia and reperfusion. In normal hearts, amrinone had no effect on myocardial contractility, heart rate, coronary perfusion pressure or left ventricular end diastolic pressure. Ischaemia–reperfusion caused an increase in coronary perfusion pressure, left ventricular end diastolic pressure and creatine kinase outflow and amrinone (present from before ischaemia) decreased the rise in all of these parameters. However, when amrinone was added only after the ischaemia, it had no effect on coronary perfusion pressure or left ventricular end diastolic pressure. Thus, the effect on coronary perfusion pressure must be due to actions during the ischaemia phase. We suggest that amrinone has pharmacological properties which may be useful in reducing ischaemia–reperfusion injury. We speculate that this involves altering ischaemia-induced changes in intracellular Ca
2+ in the myocytes.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>10958893</pmid><doi>10.1016/S0014-2999(00)00443-X</doi><tpages>8</tpages></addata></record> |
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| subjects | 1-Methyl-3-isobutylxanthine - pharmacology 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester - pharmacology Amrinone Amrinone - pharmacology Animals Biological and medical sciences Cardiotonic Agents - pharmacology Cardiovascular system Creatine Kinase - metabolism Ischaemia L-Lactate Dehydrogenase - metabolism Male Medical sciences Milrinone - pharmacology Miscellaneous Myocardial Reperfusion Injury - drug therapy Myocardial Reperfusion Injury - pathology Myocardium - pathology Pharmacology. Drug treatments Phosphodiesterase Inhibitors - pharmacology Rat Rats Rats, Sprague-Dawley Reperfusion injury Vasodilation - drug effects |
| title | Amrinone reduces ischaemia–reperfusion injury in rat heart |
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