Protective action of YM-12617, an α 1-adrenoceptor antagonist, on the hypoxic and reoxygenated myocardium
The present study was designed to determine whether the 1-form of YM-12617, which was developed recently as an α 1-adrenoceptor blocker, is capable of protecting the myocardium from hypoxia-induced disturbances of cardiac function and metabolism. Isolated rabbit hearts were perfused for 25 min under...
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| Veröffentlicht in: | European journal of pharmacology 1989-06, Vol.165 (1), p.97-106 |
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| creator | Tanonaka, K Matsumoto, M Miyake, K Minematsu, R Takeo, S |
| description | The present study was designed to determine whether the 1-form of YM-12617, which was developed recently as an α
1-adrenoceptor blocker, is capable of protecting the myocardium from hypoxia-induced disturbances of cardiac function and metabolism. Isolated rabbit hearts were perfused for 25 min under hypoxic conditions in the absence or the presence of 28 μM YM-12617, followed by 45 min with oxygenated perfusion medium, and functional and metabolic changes of the heart were examined. Hypoxia induced several pathophysiological changes. Upon subsequent reoxygenation, there was less than 10% recovery of the contractile force and an approximately 40% recovery of the myocardial high-energy phosphates. Treatment with YM-12617 during the hypoxic periods resulted in approximately 90% recovery of the cardiac contractile function upon subsequent reoxygenation. Treatment with YM-12617 restored the myocardial high-energy phosphates, such as ATP and creatine phosphate, to approximately 90 and 80% of the initial value, respectively, during the subsequent reoxygenation. These results suggest that YM-12617 is capable of protecting the myocardium from hypoxia-induced disturbances of cardiac function and metabolism. |
| doi_str_mv | 10.1016/0014-2999(89)90774-7 |
| format | Article |
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1-adrenoceptor blocker, is capable of protecting the myocardium from hypoxia-induced disturbances of cardiac function and metabolism. Isolated rabbit hearts were perfused for 25 min under hypoxic conditions in the absence or the presence of 28 μM YM-12617, followed by 45 min with oxygenated perfusion medium, and functional and metabolic changes of the heart were examined. Hypoxia induced several pathophysiological changes. Upon subsequent reoxygenation, there was less than 10% recovery of the contractile force and an approximately 40% recovery of the myocardial high-energy phosphates. Treatment with YM-12617 during the hypoxic periods resulted in approximately 90% recovery of the cardiac contractile function upon subsequent reoxygenation. Treatment with YM-12617 restored the myocardial high-energy phosphates, such as ATP and creatine phosphate, to approximately 90 and 80% of the initial value, respectively, during the subsequent reoxygenation. These results suggest that YM-12617 is capable of protecting the myocardium from hypoxia-induced disturbances of cardiac function and metabolism.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Adrenergic alpha-Antagonists - pharmacology</subject><subject>Animals</subject><subject>Body Water - metabolism</subject><subject>Calcium - blood</subject><subject>Calcium - metabolism</subject><subject>Cell membrane permeability</subject><subject>Chromatography, High Pressure Liquid</subject><subject>Coronary Circulation - drug effects</subject><subject>Creatine kinase</subject><subject>Creatine Kinase - blood</subject><subject>Creatine Kinase - metabolism</subject><subject>Heart - drug effects</subject><subject>High-energy phosphates</subject><subject>Hypoxia</subject><subject>In Vitro Techniques</subject><subject>Male</subject><subject>Myocardium - enzymology</subject><subject>Myocardium - metabolism</subject><subject>Oxygen - pharmacology</subject><subject>Perfusion</subject><subject>Rabbits</subject><subject>Reoxygenation</subject><subject>Spectrophotometry, Ultraviolet</subject><subject>Sulfonamides - pharmacology</subject><subject>Time Factors</subject><subject>YM-12617</subject><subject>α-Adrenoceptor antagonists</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1989</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9UdtKAzEQDaLUWv0DhTyJQleT7CWbF0GKN6jogz74FNJktk3pbmo2Le1n-SN-k-kFYeDAnDPDzDkInVNyQwktbgmhWcKEEFeluBaE8yzhB6hLSy4Swik7RN1_yTE6adspISQXLO-gDssLIUrWRdN37wLoYJeAVQTXYFfhr9eEsoLyPlYN_v3BNFHGQ-M0zIPzsRnU2DW2DX0cB8IE8GQ9dyurI2WwB7daj6FRAQyu104rb-yiPkVHlZq1cLbHHvp8fPgYPCfDt6eXwf0wASrSkOiKp4yZshzlWrEiVgVVWhlQnJSmLAQpWA75KCOw_SczVSoqlmea6mxEeNpDl7u9c---F9AGWdtWw2ymGnCLVnJBC15wFoUXe-FiVIORc29r5ddyb07k73Y8xGuXFrxstYVGg7E-WiaNs5ISuQlDbpyWG6dlKeQ2DMnTP3L1e3g</recordid><startdate>19890608</startdate><enddate>19890608</enddate><creator>Tanonaka, K</creator><creator>Matsumoto, M</creator><creator>Miyake, K</creator><creator>Minematsu, R</creator><creator>Takeo, S</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>19890608</creationdate><title>Protective action of YM-12617, an α 1-adrenoceptor antagonist, on the hypoxic and reoxygenated myocardium</title><author>Tanonaka, K ; Matsumoto, M ; Miyake, K ; Minematsu, R ; Takeo, S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-e193t-cf7322d88b5ca26a26fef3fdea708d8690625e5b40e000594df39f254c1c4b073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1989</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Adrenergic alpha-Antagonists - pharmacology</topic><topic>Animals</topic><topic>Body Water - metabolism</topic><topic>Calcium - blood</topic><topic>Calcium - metabolism</topic><topic>Cell membrane permeability</topic><topic>Chromatography, High Pressure Liquid</topic><topic>Coronary Circulation - drug effects</topic><topic>Creatine kinase</topic><topic>Creatine Kinase - blood</topic><topic>Creatine Kinase - metabolism</topic><topic>Heart - drug effects</topic><topic>High-energy phosphates</topic><topic>Hypoxia</topic><topic>In Vitro Techniques</topic><topic>Male</topic><topic>Myocardium - enzymology</topic><topic>Myocardium - metabolism</topic><topic>Oxygen - pharmacology</topic><topic>Perfusion</topic><topic>Rabbits</topic><topic>Reoxygenation</topic><topic>Spectrophotometry, Ultraviolet</topic><topic>Sulfonamides - pharmacology</topic><topic>Time Factors</topic><topic>YM-12617</topic><topic>α-Adrenoceptor antagonists</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tanonaka, K</creatorcontrib><creatorcontrib>Matsumoto, M</creatorcontrib><creatorcontrib>Miyake, K</creatorcontrib><creatorcontrib>Minematsu, R</creatorcontrib><creatorcontrib>Takeo, S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tanonaka, K</au><au>Matsumoto, M</au><au>Miyake, K</au><au>Minematsu, R</au><au>Takeo, S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protective action of YM-12617, an α 1-adrenoceptor antagonist, on the hypoxic and reoxygenated myocardium</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>1989-06-08</date><risdate>1989</risdate><volume>165</volume><issue>1</issue><spage>97</spage><epage>106</epage><pages>97-106</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><abstract>The present study was designed to determine whether the 1-form of YM-12617, which was developed recently as an α
1-adrenoceptor blocker, is capable of protecting the myocardium from hypoxia-induced disturbances of cardiac function and metabolism. Isolated rabbit hearts were perfused for 25 min under hypoxic conditions in the absence or the presence of 28 μM YM-12617, followed by 45 min with oxygenated perfusion medium, and functional and metabolic changes of the heart were examined. Hypoxia induced several pathophysiological changes. Upon subsequent reoxygenation, there was less than 10% recovery of the contractile force and an approximately 40% recovery of the myocardial high-energy phosphates. Treatment with YM-12617 during the hypoxic periods resulted in approximately 90% recovery of the cardiac contractile function upon subsequent reoxygenation. Treatment with YM-12617 restored the myocardial high-energy phosphates, such as ATP and creatine phosphate, to approximately 90 and 80% of the initial value, respectively, during the subsequent reoxygenation. These results suggest that YM-12617 is capable of protecting the myocardium from hypoxia-induced disturbances of cardiac function and metabolism.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>2569982</pmid><doi>10.1016/0014-2999(89)90774-7</doi><tpages>10</tpages></addata></record> |
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| ispartof | European journal of pharmacology, 1989-06, Vol.165 (1), p.97-106 |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Adenosine Triphosphate - metabolism Adrenergic alpha-Antagonists - pharmacology Animals Body Water - metabolism Calcium - blood Calcium - metabolism Cell membrane permeability Chromatography, High Pressure Liquid Coronary Circulation - drug effects Creatine kinase Creatine Kinase - blood Creatine Kinase - metabolism Heart - drug effects High-energy phosphates Hypoxia In Vitro Techniques Male Myocardium - enzymology Myocardium - metabolism Oxygen - pharmacology Perfusion Rabbits Reoxygenation Spectrophotometry, Ultraviolet Sulfonamides - pharmacology Time Factors YM-12617 α-Adrenoceptor antagonists |
| title | Protective action of YM-12617, an α 1-adrenoceptor antagonist, on the hypoxic and reoxygenated myocardium |
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