Platelet glycoprotein IIb/IIIa receptor blockade improves vascular nitric oxide bioavailability in patients with coronary artery disease
Platelet glycoprotein IIb/IIIa receptor blockade not only enhances epicardial flow but also improves microvascular perfusion. Inhibition of abnormal platelet-endothelial interactions may contribute to this beneficial effect. The present study was designed to determine whether glycoprotein IIb/IIIa r...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2003-08, Vol.108 (5), p.536-541 |
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| creator | Heitzer, Thomas Ollmann, Isabel Köke, Katharina Meinertz, Thomas Munzel, Thomas |
| description | Platelet glycoprotein IIb/IIIa receptor blockade not only enhances epicardial flow but also improves microvascular perfusion. Inhibition of abnormal platelet-endothelial interactions may contribute to this beneficial effect. The present study was designed to determine whether glycoprotein IIb/IIIa receptor blockade influences endothelial vasomotor function and NO bioactivity in patients with coronary artery disease.
Forty patients with symptomatic coronary artery stenosis were studied before planned percutaneous coronary intervention. By using venous occlusion plethysmography, endothelium-dependent and -independent vasodilation was determined by measuring forearm blood flow responses to acetylcholine with and without NG-monomethyl-L-arginine (L-NMMA) and sodium nitroprusside. Vascular function tests were repeated during glycoprotein IIb/IIIa receptor blockade by tirofiban in 27 patients and by eptifibatide in 13 patients. A subgroup of 10 patients was retested 6 hours after stopping infusion of tirofiban. Glycoprotein IIb/IIIa receptor blockade by both substances improved acetylcholine-induced vasodilation and L-NMMA responses. Six hours after withdrawal of tirofiban infusion, the beneficial effects were not evident. Sodium nitroprusside-induced vasodilation was not changed by glycoprotein IIb/IIIa receptor blockade.
These findings support the concept that abnormal platelet-endothelial interactions contribute to endothelial dysfunction and impaired NO bioactivity in patients with symptomatic coronary artery disease. |
| doi_str_mv | 10.1161/01.CIR.0000081774.31064.62 |
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Forty patients with symptomatic coronary artery stenosis were studied before planned percutaneous coronary intervention. By using venous occlusion plethysmography, endothelium-dependent and -independent vasodilation was determined by measuring forearm blood flow responses to acetylcholine with and without NG-monomethyl-L-arginine (L-NMMA) and sodium nitroprusside. Vascular function tests were repeated during glycoprotein IIb/IIIa receptor blockade by tirofiban in 27 patients and by eptifibatide in 13 patients. A subgroup of 10 patients was retested 6 hours after stopping infusion of tirofiban. Glycoprotein IIb/IIIa receptor blockade by both substances improved acetylcholine-induced vasodilation and L-NMMA responses. Six hours after withdrawal of tirofiban infusion, the beneficial effects were not evident. Sodium nitroprusside-induced vasodilation was not changed by glycoprotein IIb/IIIa receptor blockade.
These findings support the concept that abnormal platelet-endothelial interactions contribute to endothelial dysfunction and impaired NO bioactivity in patients with symptomatic coronary artery disease.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.0000081774.31064.62</identifier><identifier>PMID: 12874186</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Acetylcholine - pharmacology ; Biological Availability ; Blood Flow Velocity - drug effects ; Blood Platelets - drug effects ; Blood Platelets - metabolism ; Coronary Artery Disease - drug therapy ; Coronary Artery Disease - physiopathology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - physiopathology ; Enzyme Inhibitors - pharmacology ; Forearm - blood supply ; Humans ; Male ; Middle Aged ; Nitric Oxide - metabolism ; Nitric Oxide Donors - pharmacology ; omega-N-Methylarginine - pharmacology ; Peptides - pharmacology ; Platelet Aggregation Inhibitors - pharmacology ; Platelet Glycoprotein GPIIb-IIIa Complex - antagonists & inhibitors ; Plethysmography ; Tyrosine - analogs & derivatives ; Tyrosine - pharmacology ; Vasodilation - drug effects ; Vasodilator Agents - pharmacology ; Vasomotor System - drug effects ; Vasomotor System - physiopathology</subject><ispartof>Circulation (New York, N.Y.), 2003-08, Vol.108 (5), p.536-541</ispartof><rights>Copyright American Heart Association, Inc. Aug 5 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c435t-cabd0b3977b8b848234efdc5df31f5cbe841bbb188b2cbd2ac80765fa94f15593</citedby><cites>FETCH-LOGICAL-c435t-cabd0b3977b8b848234efdc5df31f5cbe841bbb188b2cbd2ac80765fa94f15593</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12874186$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Heitzer, Thomas</creatorcontrib><creatorcontrib>Ollmann, Isabel</creatorcontrib><creatorcontrib>Köke, Katharina</creatorcontrib><creatorcontrib>Meinertz, Thomas</creatorcontrib><creatorcontrib>Munzel, Thomas</creatorcontrib><title>Platelet glycoprotein IIb/IIIa receptor blockade improves vascular nitric oxide bioavailability in patients with coronary artery disease</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Platelet glycoprotein IIb/IIIa receptor blockade not only enhances epicardial flow but also improves microvascular perfusion. Inhibition of abnormal platelet-endothelial interactions may contribute to this beneficial effect. The present study was designed to determine whether glycoprotein IIb/IIIa receptor blockade influences endothelial vasomotor function and NO bioactivity in patients with coronary artery disease.
Forty patients with symptomatic coronary artery stenosis were studied before planned percutaneous coronary intervention. By using venous occlusion plethysmography, endothelium-dependent and -independent vasodilation was determined by measuring forearm blood flow responses to acetylcholine with and without NG-monomethyl-L-arginine (L-NMMA) and sodium nitroprusside. Vascular function tests were repeated during glycoprotein IIb/IIIa receptor blockade by tirofiban in 27 patients and by eptifibatide in 13 patients. A subgroup of 10 patients was retested 6 hours after stopping infusion of tirofiban. Glycoprotein IIb/IIIa receptor blockade by both substances improved acetylcholine-induced vasodilation and L-NMMA responses. Six hours after withdrawal of tirofiban infusion, the beneficial effects were not evident. Sodium nitroprusside-induced vasodilation was not changed by glycoprotein IIb/IIIa receptor blockade.
These findings support the concept that abnormal platelet-endothelial interactions contribute to endothelial dysfunction and impaired NO bioactivity in patients with symptomatic coronary artery disease.</description><subject>Acetylcholine - pharmacology</subject><subject>Biological Availability</subject><subject>Blood Flow Velocity - drug effects</subject><subject>Blood Platelets - drug effects</subject><subject>Blood Platelets - metabolism</subject><subject>Coronary Artery Disease - drug therapy</subject><subject>Coronary Artery Disease - physiopathology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Forearm - blood supply</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Donors - pharmacology</subject><subject>omega-N-Methylarginine - pharmacology</subject><subject>Peptides - pharmacology</subject><subject>Platelet Aggregation Inhibitors - pharmacology</subject><subject>Platelet Glycoprotein GPIIb-IIIa Complex - antagonists & inhibitors</subject><subject>Plethysmography</subject><subject>Tyrosine - analogs & derivatives</subject><subject>Tyrosine - pharmacology</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilator Agents - pharmacology</subject><subject>Vasomotor System - drug effects</subject><subject>Vasomotor System - physiopathology</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1u1DAQgC1ERZfCKyCrB25J45_YDje0oiVSJRCCs2U7E3DxxovtLOwb9LFx6UqV8GVkzTczHn8IXZKuJUSQq4602_FL2z0cRaTkLSOd4K2gz9CG9JQ3vGfDc7Sp-aGRjNJz9DLnu3oVTPYv0DmhSnKixAbdfw6mQICCv4eji_sUC_gFj6O9GsfR4AQO9iUmbEN0P80E2O8qdICMDya7NZiEF1-Sdzj-8TVtfTQH44OxPvhyxLXZ3hQPS8n4ty8_sIspLiYdsUkFaph8BpPhFTqbTcjw-hQv0LfrD1-3H5vbTzfj9v1t4zjrS-OMnTrLBimtsooryjjMk-unmZG5dxYUJ9ZaopSlzk7UONVJ0c9m4DPp-4FdoLePfesWv1bIRe98dhCCWSCuWUtWP1BJUcHL_8C7uKalvk1TQoXggvMKvXuEXIo5J5j1Pvld3U6TTj_I0h3RVZZ-kqX_ydKC1uI3pwmr3cH0VHqyw_4CmFyT_Q</recordid><startdate>20030805</startdate><enddate>20030805</enddate><creator>Heitzer, Thomas</creator><creator>Ollmann, Isabel</creator><creator>Köke, Katharina</creator><creator>Meinertz, Thomas</creator><creator>Munzel, Thomas</creator><general>American Heart Association, Inc</general><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>20030805</creationdate><title>Platelet glycoprotein IIb/IIIa receptor blockade improves vascular nitric oxide bioavailability in patients with coronary artery disease</title><author>Heitzer, Thomas ; Ollmann, Isabel ; Köke, Katharina ; Meinertz, Thomas ; Munzel, Thomas</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c435t-cabd0b3977b8b848234efdc5df31f5cbe841bbb188b2cbd2ac80765fa94f15593</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Biological Availability</topic><topic>Blood Flow Velocity - drug effects</topic><topic>Blood Platelets - drug effects</topic><topic>Blood Platelets - metabolism</topic><topic>Coronary Artery Disease - drug therapy</topic><topic>Coronary Artery Disease - physiopathology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Forearm - blood supply</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Donors - pharmacology</topic><topic>omega-N-Methylarginine - pharmacology</topic><topic>Peptides - pharmacology</topic><topic>Platelet Aggregation Inhibitors - pharmacology</topic><topic>Platelet Glycoprotein GPIIb-IIIa Complex - antagonists & inhibitors</topic><topic>Plethysmography</topic><topic>Tyrosine - analogs & derivatives</topic><topic>Tyrosine - pharmacology</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilator Agents - pharmacology</topic><topic>Vasomotor System - drug effects</topic><topic>Vasomotor System - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Heitzer, Thomas</creatorcontrib><creatorcontrib>Ollmann, Isabel</creatorcontrib><creatorcontrib>Köke, Katharina</creatorcontrib><creatorcontrib>Meinertz, Thomas</creatorcontrib><creatorcontrib>Munzel, Thomas</creatorcontrib><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>Heitzer, Thomas</au><au>Ollmann, Isabel</au><au>Köke, Katharina</au><au>Meinertz, Thomas</au><au>Munzel, Thomas</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Platelet glycoprotein IIb/IIIa receptor blockade improves vascular nitric oxide bioavailability in patients with coronary artery disease</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2003-08-05</date><risdate>2003</risdate><volume>108</volume><issue>5</issue><spage>536</spage><epage>541</epage><pages>536-541</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Platelet glycoprotein IIb/IIIa receptor blockade not only enhances epicardial flow but also improves microvascular perfusion. Inhibition of abnormal platelet-endothelial interactions may contribute to this beneficial effect. The present study was designed to determine whether glycoprotein IIb/IIIa receptor blockade influences endothelial vasomotor function and NO bioactivity in patients with coronary artery disease.
Forty patients with symptomatic coronary artery stenosis were studied before planned percutaneous coronary intervention. By using venous occlusion plethysmography, endothelium-dependent and -independent vasodilation was determined by measuring forearm blood flow responses to acetylcholine with and without NG-monomethyl-L-arginine (L-NMMA) and sodium nitroprusside. Vascular function tests were repeated during glycoprotein IIb/IIIa receptor blockade by tirofiban in 27 patients and by eptifibatide in 13 patients. A subgroup of 10 patients was retested 6 hours after stopping infusion of tirofiban. Glycoprotein IIb/IIIa receptor blockade by both substances improved acetylcholine-induced vasodilation and L-NMMA responses. Six hours after withdrawal of tirofiban infusion, the beneficial effects were not evident. Sodium nitroprusside-induced vasodilation was not changed by glycoprotein IIb/IIIa receptor blockade.
These findings support the concept that abnormal platelet-endothelial interactions contribute to endothelial dysfunction and impaired NO bioactivity in patients with symptomatic coronary artery disease.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>12874186</pmid><doi>10.1161/01.CIR.0000081774.31064.62</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 2003-08, Vol.108 (5), p.536-541 |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Acetylcholine - pharmacology Biological Availability Blood Flow Velocity - drug effects Blood Platelets - drug effects Blood Platelets - metabolism Coronary Artery Disease - drug therapy Coronary Artery Disease - physiopathology Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Endothelium, Vascular - physiopathology Enzyme Inhibitors - pharmacology Forearm - blood supply Humans Male Middle Aged Nitric Oxide - metabolism Nitric Oxide Donors - pharmacology omega-N-Methylarginine - pharmacology Peptides - pharmacology Platelet Aggregation Inhibitors - pharmacology Platelet Glycoprotein GPIIb-IIIa Complex - antagonists & inhibitors Plethysmography Tyrosine - analogs & derivatives Tyrosine - pharmacology Vasodilation - drug effects Vasodilator Agents - pharmacology Vasomotor System - drug effects Vasomotor System - physiopathology |
| title | Platelet glycoprotein IIb/IIIa receptor blockade improves vascular nitric oxide bioavailability in patients with coronary artery disease |
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