Role of nitric oxide in the coronary microvascular responses to adenosine and increased metabolic demand
The purpose of this study was to test the hypothesis that endothelium-derived nitric oxide (NO) participates in coronary microvascular responses to adenosine and pacing-induced increases in metabolic demand by maintaining an optimal distribution of coronary resistance. Coronary microvascular diamete...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 1995-03, Vol.91 (6), p.1807-1813 |
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| creator | JONES, C. J. H LIH KUO DAVIS, M. J DEFILY, D. V CHILIAN, W. M |
| description | The purpose of this study was to test the hypothesis that endothelium-derived nitric oxide (NO) participates in coronary microvascular responses to adenosine and pacing-induced increases in metabolic demand by maintaining an optimal distribution of coronary resistance.
Coronary microvascular diameters were measured by stroboscopic epi-illumination and intravital microscopy in open-chest dogs (n = 20). Epicardial coronary blood velocity (CBV) was measured by Doppler flowmetry. Responses to adenosine (1 and 10 micrograms.kg-1.min-1 IC) and left atrial pacing (180 beats per minute) were recorded before and after inhibition of NO synthesis by NG-nitro-L-arginine methyl ester (L-NAME, 30 micrograms.kg-1.min-1 IC). At baseline, adenosine dilated arterioles (< 100 microns) (11 +/- 4% and 25 +/- 3% diameter changes, P < .05) more than small arteries (> 100 microns) (-4 +/- 6% and 7 +/- 3%, P < .05 for the higher dose) and increased CBV (43 +/- 31% and 118 +/- 25%, P < .05). Left atrial pacing dilated arterioles (12 +/- 2%, P < .05) and small arteries (8 +/- 3%, P < .05) and also increased CBV (68 +/- 9%, P < .05). L-NAME abolished CBV increases caused by acetylcholine (10 and 100 ng.kg-1.min-1 IC; 53 +/- 33% and 168 +/- 82% versus -12 +/- 15% and -1 +/- 14%, P < .05) but not papaverine. Small arteries were constricted by L-NAME (-8 +/- 2%, P < .05), arterioles were dilated (10 +/- 4%, P < .05), and CBV was unchanged. After L-NAME, adenosine failed to dilate arterioles further (3 +/- 3% and 2 +/- 2%; P < .05 versus prior responses), and CBV changes were attenuated (14 +/- 16% and 8 +/- 13%; P < .05 versus prior responses). Pacing also failed to dilate arterioles (-4 +/- 2%, P < .05 versus prior response), resulting in an attenuated CBV change (34 +/- 13%, P < .05 versus prior response). The possibility that adenosine stimulates NO release in canine coronary arterioles was investigated in isolated arterioles (diameters, 81 +/- 4 microns; n = 8). Adenosine caused dose-dependent dilation to maximal diameter, which was unaffected by inhibition of NO synthesis by L-NAME.
Inhibition of NO synthesis attenuates coronary dilation during adenosine infusions and during pacing-induced increases in metabolic demand. Inhibition of NO synthesis may shift the major site of coronary resistance into small arteries through autoregulatory adjustments in arterioles. These data therefore suggest that NO, by dilating predominantly small coronary arteries, promotes metabolic coronary dila |
| doi_str_mv | 10.1161/01.cir.91.6.1807 |
| format | Article |
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Coronary microvascular diameters were measured by stroboscopic epi-illumination and intravital microscopy in open-chest dogs (n = 20). Epicardial coronary blood velocity (CBV) was measured by Doppler flowmetry. Responses to adenosine (1 and 10 micrograms.kg-1.min-1 IC) and left atrial pacing (180 beats per minute) were recorded before and after inhibition of NO synthesis by NG-nitro-L-arginine methyl ester (L-NAME, 30 micrograms.kg-1.min-1 IC). At baseline, adenosine dilated arterioles (< 100 microns) (11 +/- 4% and 25 +/- 3% diameter changes, P < .05) more than small arteries (> 100 microns) (-4 +/- 6% and 7 +/- 3%, P < .05 for the higher dose) and increased CBV (43 +/- 31% and 118 +/- 25%, P < .05). Left atrial pacing dilated arterioles (12 +/- 2%, P < .05) and small arteries (8 +/- 3%, P < .05) and also increased CBV (68 +/- 9%, P < .05). L-NAME abolished CBV increases caused by acetylcholine (10 and 100 ng.kg-1.min-1 IC; 53 +/- 33% and 168 +/- 82% versus -12 +/- 15% and -1 +/- 14%, P < .05) but not papaverine. Small arteries were constricted by L-NAME (-8 +/- 2%, P < .05), arterioles were dilated (10 +/- 4%, P < .05), and CBV was unchanged. After L-NAME, adenosine failed to dilate arterioles further (3 +/- 3% and 2 +/- 2%; P < .05 versus prior responses), and CBV changes were attenuated (14 +/- 16% and 8 +/- 13%; P < .05 versus prior responses). Pacing also failed to dilate arterioles (-4 +/- 2%, P < .05 versus prior response), resulting in an attenuated CBV change (34 +/- 13%, P < .05 versus prior response). The possibility that adenosine stimulates NO release in canine coronary arterioles was investigated in isolated arterioles (diameters, 81 +/- 4 microns; n = 8). Adenosine caused dose-dependent dilation to maximal diameter, which was unaffected by inhibition of NO synthesis by L-NAME.
Inhibition of NO synthesis attenuates coronary dilation during adenosine infusions and during pacing-induced increases in metabolic demand. Inhibition of NO synthesis may shift the major site of coronary resistance into small arteries through autoregulatory adjustments in arterioles. These data therefore suggest that NO, by dilating predominantly small coronary arteries, promotes metabolic coronary dilation by preserving the tone and vasodilator reserve of arterioles.]]></description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.cir.91.6.1807</identifier><identifier>PMID: 7882491</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Adenosine - pharmacology ; Animals ; Biological and medical sciences ; Blood Flow Velocity ; Blood Pressure - drug effects ; Cardiac Pacing, Artificial ; Coronary Circulation - drug effects ; Dogs ; Female ; Fundamental and applied biological sciences. Psychology ; Heart ; Heart Rate - drug effects ; Male ; Microcirculation - cytology ; Microcirculation - drug effects ; Myocardium - cytology ; Myocardium - metabolism ; Nitric Oxide - antagonists & inhibitors ; Nitric Oxide - physiology ; Papaverine - pharmacology ; Vascular Resistance - drug effects ; Vertebrates: cardiovascular system</subject><ispartof>Circulation (New York, N.Y.), 1995-03, Vol.91 (6), p.1807-1813</ispartof><rights>1995 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Mar 15, 1995</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-5206d2ca62fff364f0eaadab871db738f82bb35956049355636e247d2780f1cf3</citedby><cites>FETCH-LOGICAL-c504t-5206d2ca62fff364f0eaadab871db738f82bb35956049355636e247d2780f1cf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3473557$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7882491$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>JONES, C. J. H</creatorcontrib><creatorcontrib>LIH KUO</creatorcontrib><creatorcontrib>DAVIS, M. J</creatorcontrib><creatorcontrib>DEFILY, D. V</creatorcontrib><creatorcontrib>CHILIAN, W. M</creatorcontrib><title>Role of nitric oxide in the coronary microvascular responses to adenosine and increased metabolic demand</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description><![CDATA[The purpose of this study was to test the hypothesis that endothelium-derived nitric oxide (NO) participates in coronary microvascular responses to adenosine and pacing-induced increases in metabolic demand by maintaining an optimal distribution of coronary resistance.
Coronary microvascular diameters were measured by stroboscopic epi-illumination and intravital microscopy in open-chest dogs (n = 20). Epicardial coronary blood velocity (CBV) was measured by Doppler flowmetry. Responses to adenosine (1 and 10 micrograms.kg-1.min-1 IC) and left atrial pacing (180 beats per minute) were recorded before and after inhibition of NO synthesis by NG-nitro-L-arginine methyl ester (L-NAME, 30 micrograms.kg-1.min-1 IC). At baseline, adenosine dilated arterioles (< 100 microns) (11 +/- 4% and 25 +/- 3% diameter changes, P < .05) more than small arteries (> 100 microns) (-4 +/- 6% and 7 +/- 3%, P < .05 for the higher dose) and increased CBV (43 +/- 31% and 118 +/- 25%, P < .05). Left atrial pacing dilated arterioles (12 +/- 2%, P < .05) and small arteries (8 +/- 3%, P < .05) and also increased CBV (68 +/- 9%, P < .05). L-NAME abolished CBV increases caused by acetylcholine (10 and 100 ng.kg-1.min-1 IC; 53 +/- 33% and 168 +/- 82% versus -12 +/- 15% and -1 +/- 14%, P < .05) but not papaverine. Small arteries were constricted by L-NAME (-8 +/- 2%, P < .05), arterioles were dilated (10 +/- 4%, P < .05), and CBV was unchanged. After L-NAME, adenosine failed to dilate arterioles further (3 +/- 3% and 2 +/- 2%; P < .05 versus prior responses), and CBV changes were attenuated (14 +/- 16% and 8 +/- 13%; P < .05 versus prior responses). Pacing also failed to dilate arterioles (-4 +/- 2%, P < .05 versus prior response), resulting in an attenuated CBV change (34 +/- 13%, P < .05 versus prior response). The possibility that adenosine stimulates NO release in canine coronary arterioles was investigated in isolated arterioles (diameters, 81 +/- 4 microns; n = 8). Adenosine caused dose-dependent dilation to maximal diameter, which was unaffected by inhibition of NO synthesis by L-NAME.
Inhibition of NO synthesis attenuates coronary dilation during adenosine infusions and during pacing-induced increases in metabolic demand. Inhibition of NO synthesis may shift the major site of coronary resistance into small arteries through autoregulatory adjustments in arterioles. These data therefore suggest that NO, by dilating predominantly small coronary arteries, promotes metabolic coronary dilation by preserving the tone and vasodilator reserve of arterioles.]]></description><subject>Adenosine - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Flow Velocity</subject><subject>Blood Pressure - drug effects</subject><subject>Cardiac Pacing, Artificial</subject><subject>Coronary Circulation - drug effects</subject><subject>Dogs</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Heart</subject><subject>Heart Rate - drug effects</subject><subject>Male</subject><subject>Microcirculation - cytology</subject><subject>Microcirculation - drug effects</subject><subject>Myocardium - cytology</subject><subject>Myocardium - metabolism</subject><subject>Nitric Oxide - antagonists & inhibitors</subject><subject>Nitric Oxide - physiology</subject><subject>Papaverine - pharmacology</subject><subject>Vascular Resistance - drug effects</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUtr3DAUhUVJSadJ99kERCjd2dVb9rIMfQwECqFZC1m6Igq2NJXs0vz7KmTIoitxOd856J6L0BUlPaWKfia0d7H0I-1VTwei36AdlUx0QvLxDO0IIWOnOWPv0PtaH9uouJbn6FwPAxMj3aGHuzwDzgGnuJbocP4bPeCY8PoA2OWSky1PeImu5D-2um22BReox5wqVLxmbD2kXGMCbJNvRlfAVvB4gdVOeW6RHpYmXaK3wc4VPpzeC3T_7euv_Y_u9uf3w_7LbeckEWsnGVGeOatYCIErEQhY6-00aOonzYcwsGnicpSKiJFLqbgCJrRneiCBusAv0KeX3GPJvzeoq1lidTDPNkHeqtGaqsbKBt78Bz7mraT2N8MoU0IKwhtEXqC2f60FgjmWuLRKDCXm-QKGULM_3JmRGmWeL9As16fcbVrAvxpOlTf940lvfdo5FJtcrK8YF7qtpfk_Xx6OyA</recordid><startdate>19950315</startdate><enddate>19950315</enddate><creator>JONES, C. J. H</creator><creator>LIH KUO</creator><creator>DAVIS, M. J</creator><creator>DEFILY, D. V</creator><creator>CHILIAN, W. M</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</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>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>19950315</creationdate><title>Role of nitric oxide in the coronary microvascular responses to adenosine and increased metabolic demand</title><author>JONES, C. J. H ; LIH KUO ; DAVIS, M. J ; DEFILY, D. V ; CHILIAN, W. M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-5206d2ca62fff364f0eaadab871db738f82bb35956049355636e247d2780f1cf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Adenosine - pharmacology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Flow Velocity</topic><topic>Blood Pressure - drug effects</topic><topic>Cardiac Pacing, Artificial</topic><topic>Coronary Circulation - drug effects</topic><topic>Dogs</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Heart</topic><topic>Heart Rate - drug effects</topic><topic>Male</topic><topic>Microcirculation - cytology</topic><topic>Microcirculation - drug effects</topic><topic>Myocardium - cytology</topic><topic>Myocardium - metabolism</topic><topic>Nitric Oxide - antagonists & inhibitors</topic><topic>Nitric Oxide - physiology</topic><topic>Papaverine - pharmacology</topic><topic>Vascular Resistance - drug effects</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>JONES, C. J. H</creatorcontrib><creatorcontrib>LIH KUO</creatorcontrib><creatorcontrib>DAVIS, M. J</creatorcontrib><creatorcontrib>DEFILY, D. V</creatorcontrib><creatorcontrib>CHILIAN, W. M</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>JONES, C. J. H</au><au>LIH KUO</au><au>DAVIS, M. J</au><au>DEFILY, D. V</au><au>CHILIAN, W. M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of nitric oxide in the coronary microvascular responses to adenosine and increased metabolic demand</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1995-03-15</date><risdate>1995</risdate><volume>91</volume><issue>6</issue><spage>1807</spage><epage>1813</epage><pages>1807-1813</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract><![CDATA[The purpose of this study was to test the hypothesis that endothelium-derived nitric oxide (NO) participates in coronary microvascular responses to adenosine and pacing-induced increases in metabolic demand by maintaining an optimal distribution of coronary resistance.
Coronary microvascular diameters were measured by stroboscopic epi-illumination and intravital microscopy in open-chest dogs (n = 20). Epicardial coronary blood velocity (CBV) was measured by Doppler flowmetry. Responses to adenosine (1 and 10 micrograms.kg-1.min-1 IC) and left atrial pacing (180 beats per minute) were recorded before and after inhibition of NO synthesis by NG-nitro-L-arginine methyl ester (L-NAME, 30 micrograms.kg-1.min-1 IC). At baseline, adenosine dilated arterioles (< 100 microns) (11 +/- 4% and 25 +/- 3% diameter changes, P < .05) more than small arteries (> 100 microns) (-4 +/- 6% and 7 +/- 3%, P < .05 for the higher dose) and increased CBV (43 +/- 31% and 118 +/- 25%, P < .05). Left atrial pacing dilated arterioles (12 +/- 2%, P < .05) and small arteries (8 +/- 3%, P < .05) and also increased CBV (68 +/- 9%, P < .05). L-NAME abolished CBV increases caused by acetylcholine (10 and 100 ng.kg-1.min-1 IC; 53 +/- 33% and 168 +/- 82% versus -12 +/- 15% and -1 +/- 14%, P < .05) but not papaverine. Small arteries were constricted by L-NAME (-8 +/- 2%, P < .05), arterioles were dilated (10 +/- 4%, P < .05), and CBV was unchanged. After L-NAME, adenosine failed to dilate arterioles further (3 +/- 3% and 2 +/- 2%; P < .05 versus prior responses), and CBV changes were attenuated (14 +/- 16% and 8 +/- 13%; P < .05 versus prior responses). Pacing also failed to dilate arterioles (-4 +/- 2%, P < .05 versus prior response), resulting in an attenuated CBV change (34 +/- 13%, P < .05 versus prior response). The possibility that adenosine stimulates NO release in canine coronary arterioles was investigated in isolated arterioles (diameters, 81 +/- 4 microns; n = 8). Adenosine caused dose-dependent dilation to maximal diameter, which was unaffected by inhibition of NO synthesis by L-NAME.
Inhibition of NO synthesis attenuates coronary dilation during adenosine infusions and during pacing-induced increases in metabolic demand. Inhibition of NO synthesis may shift the major site of coronary resistance into small arteries through autoregulatory adjustments in arterioles. These data therefore suggest that NO, by dilating predominantly small coronary arteries, promotes metabolic coronary dilation by preserving the tone and vasodilator reserve of arterioles.]]></abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>7882491</pmid><doi>10.1161/01.cir.91.6.1807</doi><tpages>7</tpages></addata></record> |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Adenosine - pharmacology Animals Biological and medical sciences Blood Flow Velocity Blood Pressure - drug effects Cardiac Pacing, Artificial Coronary Circulation - drug effects Dogs Female Fundamental and applied biological sciences. Psychology Heart Heart Rate - drug effects Male Microcirculation - cytology Microcirculation - drug effects Myocardium - cytology Myocardium - metabolism Nitric Oxide - antagonists & inhibitors Nitric Oxide - physiology Papaverine - pharmacology Vascular Resistance - drug effects Vertebrates: cardiovascular system |
| title | Role of nitric oxide in the coronary microvascular responses to adenosine and increased metabolic demand |
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