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
Hauptverfasser: SHENG-KUN YAO, AKHTAR, S, SCOTT-BURDEN, T, OBER, J. C, GOLINO, P, BUJA, M, CASSCELLS, W, WILLERSON, J. T
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container_end_page 1010
container_issue 4
container_start_page 1005
container_title Circulation (New York, N.Y.)
container_volume 92
creator SHENG-KUN YAO
AKHTAR, S
SCOTT-BURDEN, T
OBER, J. C
GOLINO, P
BUJA, M
CASSCELLS, W
WILLERSON, J. T
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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C ; GOLINO, P ; BUJA, M ; CASSCELLS, W ; WILLERSON, J. T</creator><creatorcontrib>SHENG-KUN YAO ; AKHTAR, S ; SCOTT-BURDEN, T ; OBER, J. C ; GOLINO, P ; BUJA, M ; CASSCELLS, W ; WILLERSON, J. T</creatorcontrib><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 &lt; .01). The time to thrombus was prolonged by L-arginine (P &lt; .05) and SNP (P &lt; .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 &gt; .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 &lt; .01). The ex vivo platelet aggregation induced by collagen was inhibited after in vivo treatment with L-arginine or SNP. 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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. 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Reticuloendothelial system</subject><subject>Coronary Circulation</subject><subject>Coronary Thrombosis - blood</subject><subject>Coronary Thrombosis - prevention &amp; 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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Reticuloendothelial system</topic><topic>Coronary Circulation</topic><topic>Coronary Thrombosis - blood</topic><topic>Coronary Thrombosis - prevention &amp; 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. 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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 &lt; .01). The time to thrombus was prolonged by L-arginine (P &lt; .05) and SNP (P &lt; .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 &gt; .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 &lt; .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 &amp; 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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