Endogenous and exogenous nitric oxide protect against intracoronary thrombosis and reocclusion after thrombolysis
Nitric oxide (NO), an endothelium-derived relaxing factor, plays an important role in regulating platelet activation. We evaluated the effect of NO in a canine model of intracoronary thrombosis, thrombolysis, and reocclusion. Before thrombosis was induced, 34 anesthetized dogs were treated with a co...
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Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 1995-08, Vol.92 (4), p.1005-1010 |
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description | Nitric oxide (NO), an endothelium-derived relaxing factor, plays an important role in regulating platelet activation. We evaluated the effect of NO in a canine model of intracoronary thrombosis, thrombolysis, and reocclusion.
Before thrombosis was induced, 34 anesthetized dogs were treated with a continuous intracoronary infusion of saline (n = 8); NG-nitro-L-arginine (L-NNA, n = 8), an inhibitor of NO synthetase; L-arginine (n = 7), the precursor for NO; or sodium nitroprusside (SNP, n = 11), an NO donor. Ten minutes after the infusion was begun, an electric current of 150 microA was applied to the endothelium of coronary arteries to induce thrombosis. Occlusive thrombi developed in all dogs in the saline group (38 +/- 4 minutes) and the L-NNA group (30 +/- 6 minutes), in 6 of 7 dogs in the L-arginine group (81 +/- 18 minutes), and in 6 of 11 dogs in the SNP group (102 +/- 21 minutes) (P < .01). The time to thrombus was prolonged by L-arginine (P < .05) and SNP (P < .01). After 3 hours of thrombus formation in coronary arteries, tissue plasminogen activator and heparin were administered intravenously. Thrombi were lysed in 4 (of 8) dogs in the saline group (71 +/- 8 minutes), in 4 (of 8) dogs in the L-NNA group (72 +/- 8 minutes), in 4 (of 6) dogs in the L-arginine group (50 +/- 14 minutes), and in 4 (of 6) dogs in the SNP group (49 +/- 11 minutes) (P > .05). After thrombolysis, coronary artery reocclusion developed in all reperfused dogs in the saline group (30 +/- 8 minutes) and in the L-NNA group (48 +/- 12 minutes), in 3 (of 4) reperfused dogs in the L-arginine group (123 +/- 26 minutes), and in 3 (of 4) reperfused dogs in the SNP group (128 +/- 19 minutes) (P < .01). The ex vivo platelet aggregation induced by collagen was inhibited after in vivo treatment with L-arginine or SNP.
Increasing NO production or giving an NO donor may inhibit platelet aggregation and delay intracoronary thrombus formation and reocclusion after thrombolysis. |
doi_str_mv | 10.1161/01.CIR.92.4.1005 |
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Before thrombosis was induced, 34 anesthetized dogs were treated with a continuous intracoronary infusion of saline (n = 8); NG-nitro-L-arginine (L-NNA, n = 8), an inhibitor of NO synthetase; L-arginine (n = 7), the precursor for NO; or sodium nitroprusside (SNP, n = 11), an NO donor. Ten minutes after the infusion was begun, an electric current of 150 microA was applied to the endothelium of coronary arteries to induce thrombosis. Occlusive thrombi developed in all dogs in the saline group (38 +/- 4 minutes) and the L-NNA group (30 +/- 6 minutes), in 6 of 7 dogs in the L-arginine group (81 +/- 18 minutes), and in 6 of 11 dogs in the SNP group (102 +/- 21 minutes) (P < .01). The time to thrombus was prolonged by L-arginine (P < .05) and SNP (P < .01). After 3 hours of thrombus formation in coronary arteries, tissue plasminogen activator and heparin were administered intravenously. Thrombi were lysed in 4 (of 8) dogs in the saline group (71 +/- 8 minutes), in 4 (of 8) dogs in the L-NNA group (72 +/- 8 minutes), in 4 (of 6) dogs in the L-arginine group (50 +/- 14 minutes), and in 4 (of 6) dogs in the SNP group (49 +/- 11 minutes) (P > .05). After thrombolysis, coronary artery reocclusion developed in all reperfused dogs in the saline group (30 +/- 8 minutes) and in the L-NNA group (48 +/- 12 minutes), in 3 (of 4) reperfused dogs in the L-arginine group (123 +/- 26 minutes), and in 3 (of 4) reperfused dogs in the SNP group (128 +/- 19 minutes) (P < .01). The ex vivo platelet aggregation induced by collagen was inhibited after in vivo treatment with L-arginine or SNP.
Increasing NO production or giving an NO donor may inhibit platelet aggregation and delay intracoronary thrombus formation and reocclusion after thrombolysis.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.92.4.1005</identifier><identifier>PMID: 7641335</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Arginine - analogs & derivatives ; Arginine - pharmacology ; Biological and medical sciences ; Blood. Blood coagulation. Reticuloendothelial system ; Coronary Circulation ; Coronary Thrombosis - blood ; Coronary Thrombosis - prevention & control ; Coronary Thrombosis - therapy ; Dogs ; Electric Stimulation ; Hematocrit ; Medical sciences ; Nitric Oxide - pharmacology ; Nitric Oxide - physiology ; Nitrites - blood ; Nitroarginine ; Nitroprusside - pharmacology ; Pharmacology. Drug treatments ; Platelet Aggregation - drug effects ; Recurrence ; Thrombolytic Therapy ; Whole Blood Coagulation Time</subject><ispartof>Circulation (New York, N.Y.), 1995-08, Vol.92 (4), p.1005-1010</ispartof><rights>1995 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c364t-d3a983b16d18c15e7f6aba0084546387764d1fd32211e3616208c3f5b14122cc3</citedby><cites>FETCH-LOGICAL-c364t-d3a983b16d18c15e7f6aba0084546387764d1fd32211e3616208c3f5b14122cc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3685,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3634307$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7641335$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SHENG-KUN YAO</creatorcontrib><creatorcontrib>AKHTAR, S</creatorcontrib><creatorcontrib>SCOTT-BURDEN, T</creatorcontrib><creatorcontrib>OBER, J. C</creatorcontrib><creatorcontrib>GOLINO, P</creatorcontrib><creatorcontrib>BUJA, M</creatorcontrib><creatorcontrib>CASSCELLS, W</creatorcontrib><creatorcontrib>WILLERSON, J. T</creatorcontrib><title>Endogenous and exogenous nitric oxide protect against intracoronary thrombosis and reocclusion after thrombolysis</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Nitric oxide (NO), an endothelium-derived relaxing factor, plays an important role in regulating platelet activation. We evaluated the effect of NO in a canine model of intracoronary thrombosis, thrombolysis, and reocclusion.
Before thrombosis was induced, 34 anesthetized dogs were treated with a continuous intracoronary infusion of saline (n = 8); NG-nitro-L-arginine (L-NNA, n = 8), an inhibitor of NO synthetase; L-arginine (n = 7), the precursor for NO; or sodium nitroprusside (SNP, n = 11), an NO donor. Ten minutes after the infusion was begun, an electric current of 150 microA was applied to the endothelium of coronary arteries to induce thrombosis. Occlusive thrombi developed in all dogs in the saline group (38 +/- 4 minutes) and the L-NNA group (30 +/- 6 minutes), in 6 of 7 dogs in the L-arginine group (81 +/- 18 minutes), and in 6 of 11 dogs in the SNP group (102 +/- 21 minutes) (P < .01). The time to thrombus was prolonged by L-arginine (P < .05) and SNP (P < .01). After 3 hours of thrombus formation in coronary arteries, tissue plasminogen activator and heparin were administered intravenously. Thrombi were lysed in 4 (of 8) dogs in the saline group (71 +/- 8 minutes), in 4 (of 8) dogs in the L-NNA group (72 +/- 8 minutes), in 4 (of 6) dogs in the L-arginine group (50 +/- 14 minutes), and in 4 (of 6) dogs in the SNP group (49 +/- 11 minutes) (P > .05). After thrombolysis, coronary artery reocclusion developed in all reperfused dogs in the saline group (30 +/- 8 minutes) and in the L-NNA group (48 +/- 12 minutes), in 3 (of 4) reperfused dogs in the L-arginine group (123 +/- 26 minutes), and in 3 (of 4) reperfused dogs in the SNP group (128 +/- 19 minutes) (P < .01). The ex vivo platelet aggregation induced by collagen was inhibited after in vivo treatment with L-arginine or SNP.
Increasing NO production or giving an NO donor may inhibit platelet aggregation and delay intracoronary thrombus formation and reocclusion after thrombolysis.</description><subject>Animals</subject><subject>Arginine - analogs & derivatives</subject><subject>Arginine - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blood. Blood coagulation. Reticuloendothelial system</subject><subject>Coronary Circulation</subject><subject>Coronary Thrombosis - blood</subject><subject>Coronary Thrombosis - prevention & control</subject><subject>Coronary Thrombosis - therapy</subject><subject>Dogs</subject><subject>Electric Stimulation</subject><subject>Hematocrit</subject><subject>Medical sciences</subject><subject>Nitric Oxide - pharmacology</subject><subject>Nitric Oxide - physiology</subject><subject>Nitrites - blood</subject><subject>Nitroarginine</subject><subject>Nitroprusside - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Platelet Aggregation - drug effects</subject><subject>Recurrence</subject><subject>Thrombolytic Therapy</subject><subject>Whole Blood Coagulation Time</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>eNo9kM1LxDAQxYMoun7cvQg9iLfWTCdJ26MsfiwsCKLnkKbpGukmmmRB_3sju-tpGOb3HvMeIZdAKwABtxSq-eKl6uqKVUApPyAz4DUrGcfukMwopV3ZYF2fkNMYP_IqsOHH5LgRDBD5jHzdu8GvjPObWCg3FOZ7vzmbgtWF_7aDKT6DT0anQq2UdTEV1qWgtA_eqfBTpPfg172PdusRjNd62kTrXaHGZMIemH4yck6ORjVFc7GbZ-Tt4f51_lQunx8X87tlqVGwVA6ouhZ7EAO0GrhpRqF6RWnLOBPYNjnBAOOQswEYFCBq2moceQ8M6lprPCM3W9_8-9fGxCTXNmozTcqZnE82DWMIwDNIt6AOPsZgRvkZ7DrnkkDlX8uSgswty66WTP61nCVXO-9NvzbDv2BXa75f7-4qajWNQTlt4z-GAhnSBn8BYPWG0A</recordid><startdate>19950815</startdate><enddate>19950815</enddate><creator>SHENG-KUN YAO</creator><creator>AKHTAR, S</creator><creator>SCOTT-BURDEN, T</creator><creator>OBER, J. 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T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c364t-d3a983b16d18c15e7f6aba0084546387764d1fd32211e3616208c3f5b14122cc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Animals</topic><topic>Arginine - analogs & derivatives</topic><topic>Arginine - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blood. Blood coagulation. Reticuloendothelial system</topic><topic>Coronary Circulation</topic><topic>Coronary Thrombosis - blood</topic><topic>Coronary Thrombosis - prevention & control</topic><topic>Coronary Thrombosis - therapy</topic><topic>Dogs</topic><topic>Electric Stimulation</topic><topic>Hematocrit</topic><topic>Medical sciences</topic><topic>Nitric Oxide - pharmacology</topic><topic>Nitric Oxide - physiology</topic><topic>Nitrites - blood</topic><topic>Nitroarginine</topic><topic>Nitroprusside - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Platelet Aggregation - drug effects</topic><topic>Recurrence</topic><topic>Thrombolytic Therapy</topic><topic>Whole Blood Coagulation Time</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SHENG-KUN YAO</creatorcontrib><creatorcontrib>AKHTAR, S</creatorcontrib><creatorcontrib>SCOTT-BURDEN, T</creatorcontrib><creatorcontrib>OBER, J. C</creatorcontrib><creatorcontrib>GOLINO, P</creatorcontrib><creatorcontrib>BUJA, M</creatorcontrib><creatorcontrib>CASSCELLS, W</creatorcontrib><creatorcontrib>WILLERSON, J. 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T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endogenous and exogenous nitric oxide protect against intracoronary thrombosis and reocclusion after thrombolysis</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1995-08-15</date><risdate>1995</risdate><volume>92</volume><issue>4</issue><spage>1005</spage><epage>1010</epage><pages>1005-1010</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Nitric oxide (NO), an endothelium-derived relaxing factor, plays an important role in regulating platelet activation. We evaluated the effect of NO in a canine model of intracoronary thrombosis, thrombolysis, and reocclusion.
Before thrombosis was induced, 34 anesthetized dogs were treated with a continuous intracoronary infusion of saline (n = 8); NG-nitro-L-arginine (L-NNA, n = 8), an inhibitor of NO synthetase; L-arginine (n = 7), the precursor for NO; or sodium nitroprusside (SNP, n = 11), an NO donor. Ten minutes after the infusion was begun, an electric current of 150 microA was applied to the endothelium of coronary arteries to induce thrombosis. Occlusive thrombi developed in all dogs in the saline group (38 +/- 4 minutes) and the L-NNA group (30 +/- 6 minutes), in 6 of 7 dogs in the L-arginine group (81 +/- 18 minutes), and in 6 of 11 dogs in the SNP group (102 +/- 21 minutes) (P < .01). The time to thrombus was prolonged by L-arginine (P < .05) and SNP (P < .01). After 3 hours of thrombus formation in coronary arteries, tissue plasminogen activator and heparin were administered intravenously. Thrombi were lysed in 4 (of 8) dogs in the saline group (71 +/- 8 minutes), in 4 (of 8) dogs in the L-NNA group (72 +/- 8 minutes), in 4 (of 6) dogs in the L-arginine group (50 +/- 14 minutes), and in 4 (of 6) dogs in the SNP group (49 +/- 11 minutes) (P > .05). After thrombolysis, coronary artery reocclusion developed in all reperfused dogs in the saline group (30 +/- 8 minutes) and in the L-NNA group (48 +/- 12 minutes), in 3 (of 4) reperfused dogs in the L-arginine group (123 +/- 26 minutes), and in 3 (of 4) reperfused dogs in the SNP group (128 +/- 19 minutes) (P < .01). The ex vivo platelet aggregation induced by collagen was inhibited after in vivo treatment with L-arginine or SNP.
Increasing NO production or giving an NO donor may inhibit platelet aggregation and delay intracoronary thrombus formation and reocclusion after thrombolysis.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>7641335</pmid><doi>10.1161/01.CIR.92.4.1005</doi><tpages>6</tpages></addata></record> |
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source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
subjects | Animals Arginine - analogs & derivatives Arginine - pharmacology Biological and medical sciences Blood. Blood coagulation. Reticuloendothelial system Coronary Circulation Coronary Thrombosis - blood Coronary Thrombosis - prevention & control Coronary Thrombosis - therapy Dogs Electric Stimulation Hematocrit Medical sciences Nitric Oxide - pharmacology Nitric Oxide - physiology Nitrites - blood Nitroarginine Nitroprusside - pharmacology Pharmacology. Drug treatments Platelet Aggregation - drug effects Recurrence Thrombolytic Therapy Whole Blood Coagulation Time |
title | Endogenous and exogenous nitric oxide protect against intracoronary thrombosis and reocclusion after thrombolysis |
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