Endothelial control of coronary flow in perfused guinea pig heart
In perfused isolated guinea pig hearts reactive hyperemia (RH) was induced by occlusion of coronary flow for periods ranging from 1-60 s. RH was hampered by 100-60% in the presence of an inhibitor of NO synthase, NG-nitro-L-arginine (100 microM) and, to a lesser extent (up to 35%), by an antagonist...
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| Veröffentlicht in: | Basic research in cardiology 1995-03, Vol.90 (2), p.119-124 |
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| creator | GRYGLEWSKI, R. J CHLOPICKI, S NIEZABITOWSKI, P |
| description | In perfused isolated guinea pig hearts reactive hyperemia (RH) was induced by occlusion of coronary flow for periods ranging from 1-60 s. RH was hampered by 100-60% in the presence of an inhibitor of NO synthase, NG-nitro-L-arginine (100 microM) and, to a lesser extent (up to 35%), by an antagonist of adenosine receptors, 8-phenyltheophylline (10 microM). An inhibitor of PGH synthase, indomethacin (5 microM), did not affect RH. During RH the heart generated prostacyclin, nitric oxide, and adenosine as indicated by the appearance of 6-keto-PGF1 alpha, cyclic GMP, urate, inosine, hypoxanthine and xanthine in the perfusate. Out of these factors only NO and adenosine were responsible for RH. NO was responsible for RH which was evoked by short-term (1-10s) coronary occlusion, whereas concurrent efforts of NO and adenosine were required to maintain RH that followed longer (20-60s) periods of interruption of coronary inflow. Thus, in the investigated system nitric oxide and adenosine but not prostacyclin can be considered as the mediators of myocardial reactive hyperemia. |
| doi_str_mv | 10.1007/BF00789442 |
| format | Article |
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NO was responsible for RH which was evoked by short-term (1-10s) coronary occlusion, whereas concurrent efforts of NO and adenosine were required to maintain RH that followed longer (20-60s) periods of interruption of coronary inflow. Thus, in the investigated system nitric oxide and adenosine but not prostacyclin can be considered as the mediators of myocardial reactive hyperemia.</description><identifier>ISSN: 0300-8428</identifier><identifier>EISSN: 1435-1803</identifier><identifier>DOI: 10.1007/BF00789442</identifier><identifier>PMID: 7646416</identifier><identifier>CODEN: BRCAB7</identifier><language>eng</language><publisher>Heidelberg: Springer</publisher><subject>6-Ketoprostaglandin F1 alpha - metabolism ; Animals ; Biological and medical sciences ; Coronary Circulation - drug effects ; Coronary Circulation - physiology ; Cyclic GMP - metabolism ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - physiopathology ; Fundamental and applied biological sciences. Psychology ; Guinea Pigs ; Heart ; Hyperemia - physiopathology ; Indomethacin - pharmacology ; Nitric Oxide - antagonists & inhibitors ; Nitric Oxide - biosynthesis ; Perfusion ; Purinergic P1 Receptor Antagonists ; Purines - metabolism ; Theophylline - analogs & derivatives ; Theophylline - pharmacology ; Vertebrates: cardiovascular system</subject><ispartof>Basic research in cardiology, 1995-03, Vol.90 (2), p.119-124</ispartof><rights>1995 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c311t-270b72b52e3dc0deee6a0084a341f6c1fc9d1ff218efd622ba67ca428587c2693</citedby><cites>FETCH-LOGICAL-c311t-270b72b52e3dc0deee6a0084a341f6c1fc9d1ff218efd622ba67ca428587c2693</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,776,780,785,786,23909,23910,25118,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3514527$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7646416$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GRYGLEWSKI, R. J</creatorcontrib><creatorcontrib>CHLOPICKI, S</creatorcontrib><creatorcontrib>NIEZABITOWSKI, P</creatorcontrib><title>Endothelial control of coronary flow in perfused guinea pig heart</title><title>Basic research in cardiology</title><addtitle>Basic Res Cardiol</addtitle><description>In perfused isolated guinea pig hearts reactive hyperemia (RH) was induced by occlusion of coronary flow for periods ranging from 1-60 s. RH was hampered by 100-60% in the presence of an inhibitor of NO synthase, NG-nitro-L-arginine (100 microM) and, to a lesser extent (up to 35%), by an antagonist of adenosine receptors, 8-phenyltheophylline (10 microM). An inhibitor of PGH synthase, indomethacin (5 microM), did not affect RH. During RH the heart generated prostacyclin, nitric oxide, and adenosine as indicated by the appearance of 6-keto-PGF1 alpha, cyclic GMP, urate, inosine, hypoxanthine and xanthine in the perfusate. Out of these factors only NO and adenosine were responsible for RH. NO was responsible for RH which was evoked by short-term (1-10s) coronary occlusion, whereas concurrent efforts of NO and adenosine were required to maintain RH that followed longer (20-60s) periods of interruption of coronary inflow. Thus, in the investigated system nitric oxide and adenosine but not prostacyclin can be considered as the mediators of myocardial reactive hyperemia.</description><subject>6-Ketoprostaglandin F1 alpha - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Coronary Circulation - drug effects</subject><subject>Coronary Circulation - physiology</subject><subject>Cyclic GMP - metabolism</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Guinea Pigs</subject><subject>Heart</subject><subject>Hyperemia - physiopathology</subject><subject>Indomethacin - pharmacology</subject><subject>Nitric Oxide - antagonists & inhibitors</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Perfusion</subject><subject>Purinergic P1 Receptor Antagonists</subject><subject>Purines - metabolism</subject><subject>Theophylline - analogs & derivatives</subject><subject>Theophylline - pharmacology</subject><subject>Vertebrates: cardiovascular system</subject><issn>0300-8428</issn><issn>1435-1803</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1LAzEQhoMotVYv3oUcxIOwmq9NtsdaWhUKXvS8ZLOTdiXdrMku4r830qXCMDPwPszHi9A1JQ-UEPX4tE65mAvBTtCUCp5ntCD8FE0JJyQrBCvO0UWMn4RQISWdoImSQgoqp2ixamvf78A12mHj2z54h71NbfCtDj_YOv-NmxZ3EOwQocbboWlB467Z4h3o0F-iM6tdhKuxztDHevW-fMk2b8-vy8UmM5zSPmOKVIpVOQNeG1IDgNSEFEJzQa001Jp5Ta1ltABbS8YqLZXR6fS8UIbJOZ-hu8PcLvivAWJf7ptowDndgh9iqZTIU7AE3h9AE3yMAWzZhWaffikpKf_8Kv_9SvDNOHWo9lAf0dGgpN-Ouo5GOxt0a5p4xHhO00rFfwH3uHEw</recordid><startdate>19950301</startdate><enddate>19950301</enddate><creator>GRYGLEWSKI, R. 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J ; CHLOPICKI, S ; NIEZABITOWSKI, P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c311t-270b72b52e3dc0deee6a0084a341f6c1fc9d1ff218efd622ba67ca428587c2693</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>6-Ketoprostaglandin F1 alpha - metabolism</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Coronary Circulation - drug effects</topic><topic>Coronary Circulation - physiology</topic><topic>Cyclic GMP - metabolism</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Guinea Pigs</topic><topic>Heart</topic><topic>Hyperemia - physiopathology</topic><topic>Indomethacin - pharmacology</topic><topic>Nitric Oxide - antagonists & inhibitors</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Perfusion</topic><topic>Purinergic P1 Receptor Antagonists</topic><topic>Purines - metabolism</topic><topic>Theophylline - analogs & derivatives</topic><topic>Theophylline - pharmacology</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GRYGLEWSKI, R. J</creatorcontrib><creatorcontrib>CHLOPICKI, S</creatorcontrib><creatorcontrib>NIEZABITOWSKI, P</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>Basic research in cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GRYGLEWSKI, R. J</au><au>CHLOPICKI, S</au><au>NIEZABITOWSKI, P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endothelial control of coronary flow in perfused guinea pig heart</atitle><jtitle>Basic research in cardiology</jtitle><addtitle>Basic Res Cardiol</addtitle><date>1995-03-01</date><risdate>1995</risdate><volume>90</volume><issue>2</issue><spage>119</spage><epage>124</epage><pages>119-124</pages><issn>0300-8428</issn><eissn>1435-1803</eissn><coden>BRCAB7</coden><abstract>In perfused isolated guinea pig hearts reactive hyperemia (RH) was induced by occlusion of coronary flow for periods ranging from 1-60 s. RH was hampered by 100-60% in the presence of an inhibitor of NO synthase, NG-nitro-L-arginine (100 microM) and, to a lesser extent (up to 35%), by an antagonist of adenosine receptors, 8-phenyltheophylline (10 microM). An inhibitor of PGH synthase, indomethacin (5 microM), did not affect RH. During RH the heart generated prostacyclin, nitric oxide, and adenosine as indicated by the appearance of 6-keto-PGF1 alpha, cyclic GMP, urate, inosine, hypoxanthine and xanthine in the perfusate. Out of these factors only NO and adenosine were responsible for RH. NO was responsible for RH which was evoked by short-term (1-10s) coronary occlusion, whereas concurrent efforts of NO and adenosine were required to maintain RH that followed longer (20-60s) periods of interruption of coronary inflow. Thus, in the investigated system nitric oxide and adenosine but not prostacyclin can be considered as the mediators of myocardial reactive hyperemia.</abstract><cop>Heidelberg</cop><pub>Springer</pub><pmid>7646416</pmid><doi>10.1007/BF00789442</doi><tpages>6</tpages></addata></record> |
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| ispartof | Basic research in cardiology, 1995-03, Vol.90 (2), p.119-124 |
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| subjects | 6-Ketoprostaglandin F1 alpha - metabolism Animals Biological and medical sciences Coronary Circulation - drug effects Coronary Circulation - physiology Cyclic GMP - metabolism Endothelium, Vascular - drug effects Endothelium, Vascular - physiopathology Fundamental and applied biological sciences. Psychology Guinea Pigs Heart Hyperemia - physiopathology Indomethacin - pharmacology Nitric Oxide - antagonists & inhibitors Nitric Oxide - biosynthesis Perfusion Purinergic P1 Receptor Antagonists Purines - metabolism Theophylline - analogs & derivatives Theophylline - pharmacology Vertebrates: cardiovascular system |
| title | Endothelial control of coronary flow in perfused guinea pig heart |
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