Defibrotide, an antithrombotic substance which prevents myocardial contracture in ischemic rabbit heart
Defibrotide, a polydeoxyribonucleotide obtained from mammalian lungs, reduced in a dose-dependent fashion the ischemic contracture due to low perfusion (0.2 ml/min) of isovolumic left heart of rabbit and abolished the irregular rhytym of the heart, thereby restoring the cardiomechanical activity upo...
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| Veröffentlicht in: | European journal of pharmacology 1987-03, Vol.135 (3), p.375-382 |
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| container_title | European journal of pharmacology |
| container_volume | 135 |
| creator | Berti, Ferruccio Rossoni, Giuseppe Omini, Claudio Folco, Giancarlo Daffonchio, Luisa Viganó, Teresa Tondo, Claudio |
| description | Defibrotide, a polydeoxyribonucleotide obtained from mammalian lungs, reduced in a dose-dependent fashion the ischemic contracture due to low perfusion (0.2 ml/min) of isovolumic left heart of rabbit and abolished the irregular rhytym of the heart, thereby restoring the cardiomechanical activity upon reperfusion (20 ml/min). Defibrotide stimulated the release of PG-like material from the heart in a dose-dependent manner without modifying the basal contractility. Both PGE
2 and PGI
2 (10 ng/ml) have an antiischemic activity on this preparation as shown by the partial reduction of the ischemic contracture and by the improvement of heart contractility upon reperfusion. Indomethacin infusion (1 μg/ml) completely removed both the antiischemic activity of Defibrotide (400 μg/ml) and its ability to increase the generation of prostaglandins in the rabbit heart. These results suggest that Defibrotide has a beneficial influence on ischemic rabbit heart through an increase in prostaglandin synthesis. However other mechanisms not necessarily related to prostaglandin generation, such as direct effect on membrane function deactivation and mitochondrial Ca
2+ overload, should be considered in explaining the antiischemic activity of Defibrotide in the rabbit heart. |
| doi_str_mv | 10.1016/0014-2999(87)90687-X |
| format | Article |
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2 and PGI
2 (10 ng/ml) have an antiischemic activity on this preparation as shown by the partial reduction of the ischemic contracture and by the improvement of heart contractility upon reperfusion. Indomethacin infusion (1 μg/ml) completely removed both the antiischemic activity of Defibrotide (400 μg/ml) and its ability to increase the generation of prostaglandins in the rabbit heart. These results suggest that Defibrotide has a beneficial influence on ischemic rabbit heart through an increase in prostaglandin synthesis. However other mechanisms not necessarily related to prostaglandin generation, such as direct effect on membrane function deactivation and mitochondrial Ca
2+ overload, should be considered in explaining the antiischemic activity of Defibrotide in the rabbit heart.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/0014-2999(87)90687-X</identifier><identifier>PMID: 3556200</identifier><identifier>CODEN: EJPHAZ</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Animals ; Biological and medical sciences ; Blood. Blood coagulation. Reticuloendothelial system ; Coronary Disease - physiopathology ; Defibrotide ; Dinoprostone ; Epoprostenol - pharmacology ; Fibrinolytic Agents - pharmacology ; In Vitro Techniques ; Indomethacin ; Indomethacin - pharmacology ; Male ; Medical sciences ; Myocardial Contraction - drug effects ; Myocardial ischemia ; Pharmacology. Drug treatments ; Platelet Aggregation - drug effects ; Polydeoxyribonucleotides - pharmacology ; Prostaglandins ; Prostaglandins E - pharmacology ; Rabbits</subject><ispartof>European journal of pharmacology, 1987-03, Vol.135 (3), p.375-382</ispartof><rights>1987</rights><rights>1988 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c386t-d137cbde1ec236fa420461818ce3992307b0a58b762884e230dbcdf33b8dd773</citedby><cites>FETCH-LOGICAL-c386t-d137cbde1ec236fa420461818ce3992307b0a58b762884e230dbcdf33b8dd773</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/001429998790687X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7531276$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3556200$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Berti, Ferruccio</creatorcontrib><creatorcontrib>Rossoni, Giuseppe</creatorcontrib><creatorcontrib>Omini, Claudio</creatorcontrib><creatorcontrib>Folco, Giancarlo</creatorcontrib><creatorcontrib>Daffonchio, Luisa</creatorcontrib><creatorcontrib>Viganó, Teresa</creatorcontrib><creatorcontrib>Tondo, Claudio</creatorcontrib><title>Defibrotide, an antithrombotic substance which prevents myocardial contracture in ischemic rabbit heart</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>Defibrotide, a polydeoxyribonucleotide obtained from mammalian lungs, reduced in a dose-dependent fashion the ischemic contracture due to low perfusion (0.2 ml/min) of isovolumic left heart of rabbit and abolished the irregular rhytym of the heart, thereby restoring the cardiomechanical activity upon reperfusion (20 ml/min). Defibrotide stimulated the release of PG-like material from the heart in a dose-dependent manner without modifying the basal contractility. Both PGE
2 and PGI
2 (10 ng/ml) have an antiischemic activity on this preparation as shown by the partial reduction of the ischemic contracture and by the improvement of heart contractility upon reperfusion. Indomethacin infusion (1 μg/ml) completely removed both the antiischemic activity of Defibrotide (400 μg/ml) and its ability to increase the generation of prostaglandins in the rabbit heart. These results suggest that Defibrotide has a beneficial influence on ischemic rabbit heart through an increase in prostaglandin synthesis. However other mechanisms not necessarily related to prostaglandin generation, such as direct effect on membrane function deactivation and mitochondrial Ca
2+ overload, should be considered in explaining the antiischemic activity of Defibrotide in the rabbit heart.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood. Blood coagulation. Reticuloendothelial system</subject><subject>Coronary Disease - physiopathology</subject><subject>Defibrotide</subject><subject>Dinoprostone</subject><subject>Epoprostenol - pharmacology</subject><subject>Fibrinolytic Agents - pharmacology</subject><subject>In Vitro Techniques</subject><subject>Indomethacin</subject><subject>Indomethacin - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocardial ischemia</subject><subject>Pharmacology. Drug treatments</subject><subject>Platelet Aggregation - drug effects</subject><subject>Polydeoxyribonucleotides - pharmacology</subject><subject>Prostaglandins</subject><subject>Prostaglandins E - pharmacology</subject><subject>Rabbits</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1987</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kF1LHTEQhoMo9mj9BxVyUYpC1-ZjN8neFIqtVRC88cK7kI9ZN2U_TpOs4r9vTs_hXAoDAzPPOwwPQp8ouaKEim-E0LpibdteKHnZEqFk9XSAVlTJtiKSskO02iMf0ElKfwghTcuaY3TMm0YwQlbo-Sd0wcY5Bw9fsZlK5ZD7OI-2zBxOi03ZTA7wax9cj9cRXmDKCY9vszPRBzNgN085GpeXCDhMOCTXw1iy0VgbMu7BxPwRHXVmSHC266fo8ebX4_Vtdf_w--76x33luBK58pRLZz1QcIyLztSM1IIqqhzwtmWcSEtMo6wUTKkaysBb5zvOrfJeSn6KvmzPruP8d4GU9VjegWEwE8xL0lI2VIlmA9Zb0MU5pQidXscwmvimKdEbvXrjTm_caSX1f736qcTOd_cXO4Lfh3Y-y_7zbm-SM0MXi7qQ9phsOGVSFOz7FoOi4iVA1MkFKJZ9iOCy9nN4_49_-VCYVg</recordid><startdate>19870331</startdate><enddate>19870331</enddate><creator>Berti, Ferruccio</creator><creator>Rossoni, Giuseppe</creator><creator>Omini, Claudio</creator><creator>Folco, Giancarlo</creator><creator>Daffonchio, Luisa</creator><creator>Viganó, Teresa</creator><creator>Tondo, Claudio</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>19870331</creationdate><title>Defibrotide, an antithrombotic substance which prevents myocardial contracture in ischemic rabbit heart</title><author>Berti, Ferruccio ; Rossoni, Giuseppe ; Omini, Claudio ; Folco, Giancarlo ; Daffonchio, Luisa ; Viganó, Teresa ; Tondo, Claudio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c386t-d137cbde1ec236fa420461818ce3992307b0a58b762884e230dbcdf33b8dd773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1987</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood. Blood coagulation. Reticuloendothelial system</topic><topic>Coronary Disease - physiopathology</topic><topic>Defibrotide</topic><topic>Dinoprostone</topic><topic>Epoprostenol - pharmacology</topic><topic>Fibrinolytic Agents - pharmacology</topic><topic>In Vitro Techniques</topic><topic>Indomethacin</topic><topic>Indomethacin - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocardial ischemia</topic><topic>Pharmacology. Drug treatments</topic><topic>Platelet Aggregation - drug effects</topic><topic>Polydeoxyribonucleotides - pharmacology</topic><topic>Prostaglandins</topic><topic>Prostaglandins E - pharmacology</topic><topic>Rabbits</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Berti, Ferruccio</creatorcontrib><creatorcontrib>Rossoni, Giuseppe</creatorcontrib><creatorcontrib>Omini, Claudio</creatorcontrib><creatorcontrib>Folco, Giancarlo</creatorcontrib><creatorcontrib>Daffonchio, Luisa</creatorcontrib><creatorcontrib>Viganó, Teresa</creatorcontrib><creatorcontrib>Tondo, Claudio</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>Berti, Ferruccio</au><au>Rossoni, Giuseppe</au><au>Omini, Claudio</au><au>Folco, Giancarlo</au><au>Daffonchio, Luisa</au><au>Viganó, Teresa</au><au>Tondo, Claudio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Defibrotide, an antithrombotic substance which prevents myocardial contracture in ischemic rabbit heart</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>1987-03-31</date><risdate>1987</risdate><volume>135</volume><issue>3</issue><spage>375</spage><epage>382</epage><pages>375-382</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>Defibrotide, a polydeoxyribonucleotide obtained from mammalian lungs, reduced in a dose-dependent fashion the ischemic contracture due to low perfusion (0.2 ml/min) of isovolumic left heart of rabbit and abolished the irregular rhytym of the heart, thereby restoring the cardiomechanical activity upon reperfusion (20 ml/min). Defibrotide stimulated the release of PG-like material from the heart in a dose-dependent manner without modifying the basal contractility. Both PGE
2 and PGI
2 (10 ng/ml) have an antiischemic activity on this preparation as shown by the partial reduction of the ischemic contracture and by the improvement of heart contractility upon reperfusion. Indomethacin infusion (1 μg/ml) completely removed both the antiischemic activity of Defibrotide (400 μg/ml) and its ability to increase the generation of prostaglandins in the rabbit heart. These results suggest that Defibrotide has a beneficial influence on ischemic rabbit heart through an increase in prostaglandin synthesis. However other mechanisms not necessarily related to prostaglandin generation, such as direct effect on membrane function deactivation and mitochondrial Ca
2+ overload, should be considered in explaining the antiischemic activity of Defibrotide in the rabbit heart.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>3556200</pmid><doi>10.1016/0014-2999(87)90687-X</doi><tpages>8</tpages></addata></record> |
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| ispartof | European journal of pharmacology, 1987-03, Vol.135 (3), p.375-382 |
| issn | 0014-2999 1879-0712 |
| language | eng |
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| subjects | Animals Biological and medical sciences Blood. Blood coagulation. Reticuloendothelial system Coronary Disease - physiopathology Defibrotide Dinoprostone Epoprostenol - pharmacology Fibrinolytic Agents - pharmacology In Vitro Techniques Indomethacin Indomethacin - pharmacology Male Medical sciences Myocardial Contraction - drug effects Myocardial ischemia Pharmacology. Drug treatments Platelet Aggregation - drug effects Polydeoxyribonucleotides - pharmacology Prostaglandins Prostaglandins E - pharmacology Rabbits |
| title | Defibrotide, an antithrombotic substance which prevents myocardial contracture in ischemic rabbit heart |
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