Aspirin, But Not Clopidogrel, Reduces Collateral Conductance in a Rabbit Model of Femoral Artery Occlusion
The objective of this study was to test the potential of aspirin and clopidogrel to influence collateral artery growth (arteriogenesis). Aspirin and clopidogrel are antiplatelet agents commonly used in the treatment of ischemic cardiovascular disease. Both inhibit platelet aggregation; however, they...
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| Veröffentlicht in: | Journal of the American College of Cardiology 2005-09, Vol.46 (6), p.994-1001 |
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| creator | Hoefer, Imo E. Grundmann, Sebastian Schirmer, Stephan van Royen, Niels Meder, Benjamin Bode, Christoph Piek, Jan J. Buschmann, Ivo R. |
| description | The objective of this study was to test the potential of aspirin and clopidogrel to influence collateral artery growth (arteriogenesis).
Aspirin and clopidogrel are antiplatelet agents commonly used in the treatment of ischemic cardiovascular disease. Both inhibit platelet aggregation; however, they differ mechanistically because aspirin acts via cyclooxygenase (COX) inhibition, while clopidogrel noncompetitively antagonizes the P2Y12adenosine diphosphate receptor. We hypothesized that aspirin, due to its anti-inflammatory effects through inhibition of COX activity could inhibit arteriogenesis. Given that clopidogrel does not affect COX activity, it would be less likely to interfere with collateral artery growth.
Fifty-four New Zealand White rabbits received either saline, aspirin (10 mg/kg), or clopidogrel (10 mg/kg) for seven days after femoral artery ligation. Maximal collateral conductance was assessed with fluorescent microspheres under maximal vasodilation; cellular migration and proliferation (Ki-67) was evaluated by quantitative immunohistology.
Collateral conductance was significantly reduced by aspirin treatment, whereas clopidogrel had a neutral effect (saline: 0.94 ± 0.04; clopidogrel: 0.94 ± 0.05; aspirin: 0.64 ± 0.03 ml·min−1·100 mm Hg−1·g−1; p < 0.001). Ki-67 proliferation indexes were consistent with these results (saline: 23.1 ± 2.9%; clopidogrel: 23.5 ± 1.1%; aspirin: 19.2 ± 1.1% Ki-67–positive cells). Immunohistochemistry showed COX expression in collateral arteries and a significantly decreased monocyte/macrophage accumulation in the perivascular tissue after aspirin treatment. Cell adhesion molecule expression on monocytes after activation was significantly reduced by aspirin, which might explain the reduced migratory ability.
In summary, clopidogrel had a neutral effect on natural arteriogenesis. Aspirin significantly inhibited collateral artery growth, probably due to its anti-inflammatory effect. Additional studies are needed to substantiate these results before translation into clinical practice. |
| doi_str_mv | 10.1016/j.jacc.2005.02.094 |
| format | Article |
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Aspirin and clopidogrel are antiplatelet agents commonly used in the treatment of ischemic cardiovascular disease. Both inhibit platelet aggregation; however, they differ mechanistically because aspirin acts via cyclooxygenase (COX) inhibition, while clopidogrel noncompetitively antagonizes the P2Y12adenosine diphosphate receptor. We hypothesized that aspirin, due to its anti-inflammatory effects through inhibition of COX activity could inhibit arteriogenesis. Given that clopidogrel does not affect COX activity, it would be less likely to interfere with collateral artery growth.
Fifty-four New Zealand White rabbits received either saline, aspirin (10 mg/kg), or clopidogrel (10 mg/kg) for seven days after femoral artery ligation. Maximal collateral conductance was assessed with fluorescent microspheres under maximal vasodilation; cellular migration and proliferation (Ki-67) was evaluated by quantitative immunohistology.
Collateral conductance was significantly reduced by aspirin treatment, whereas clopidogrel had a neutral effect (saline: 0.94 ± 0.04; clopidogrel: 0.94 ± 0.05; aspirin: 0.64 ± 0.03 ml·min−1·100 mm Hg−1·g−1; p < 0.001). Ki-67 proliferation indexes were consistent with these results (saline: 23.1 ± 2.9%; clopidogrel: 23.5 ± 1.1%; aspirin: 19.2 ± 1.1% Ki-67–positive cells). Immunohistochemistry showed COX expression in collateral arteries and a significantly decreased monocyte/macrophage accumulation in the perivascular tissue after aspirin treatment. Cell adhesion molecule expression on monocytes after activation was significantly reduced by aspirin, which might explain the reduced migratory ability.
In summary, clopidogrel had a neutral effect on natural arteriogenesis. Aspirin significantly inhibited collateral artery growth, probably due to its anti-inflammatory effect. Additional studies are needed to substantiate these results before translation into clinical practice.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/j.jacc.2005.02.094</identifier><identifier>PMID: 16168281</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Arterial Occlusive Diseases - drug therapy ; Arterial Occlusive Diseases - physiopathology ; Aspirin ; Aspirin - therapeutic use ; Blood platelets ; Blood pressure ; Cardiology ; Cardiovascular disease ; Cell adhesion & migration ; Cytokines ; Disease Models, Animal ; Electrophysiology ; Endothelium ; Femoral Artery - drug effects ; Femoral Artery - physiopathology ; Laboratory animals ; Mortality ; Rabbits ; Studies ; Ticlopidine - analogs & derivatives ; Ticlopidine - therapeutic use ; Veins & arteries</subject><ispartof>Journal of the American College of Cardiology, 2005-09, Vol.46 (6), p.994-1001</ispartof><rights>2005 American College of Cardiology Foundation</rights><rights>Copyright Elsevier Limited Sep 20, 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c460t-212919b0d730839a0a27d3492f4c9205df565e5dc7523658334381156802f2473</citedby><cites>FETCH-LOGICAL-c460t-212919b0d730839a0a27d3492f4c9205df565e5dc7523658334381156802f2473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jacc.2005.02.094$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16168281$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hoefer, Imo E.</creatorcontrib><creatorcontrib>Grundmann, Sebastian</creatorcontrib><creatorcontrib>Schirmer, Stephan</creatorcontrib><creatorcontrib>van Royen, Niels</creatorcontrib><creatorcontrib>Meder, Benjamin</creatorcontrib><creatorcontrib>Bode, Christoph</creatorcontrib><creatorcontrib>Piek, Jan J.</creatorcontrib><creatorcontrib>Buschmann, Ivo R.</creatorcontrib><title>Aspirin, But Not Clopidogrel, Reduces Collateral Conductance in a Rabbit Model of Femoral Artery Occlusion</title><title>Journal of the American College of Cardiology</title><addtitle>J Am Coll Cardiol</addtitle><description>The objective of this study was to test the potential of aspirin and clopidogrel to influence collateral artery growth (arteriogenesis).
Aspirin and clopidogrel are antiplatelet agents commonly used in the treatment of ischemic cardiovascular disease. Both inhibit platelet aggregation; however, they differ mechanistically because aspirin acts via cyclooxygenase (COX) inhibition, while clopidogrel noncompetitively antagonizes the P2Y12adenosine diphosphate receptor. We hypothesized that aspirin, due to its anti-inflammatory effects through inhibition of COX activity could inhibit arteriogenesis. Given that clopidogrel does not affect COX activity, it would be less likely to interfere with collateral artery growth.
Fifty-four New Zealand White rabbits received either saline, aspirin (10 mg/kg), or clopidogrel (10 mg/kg) for seven days after femoral artery ligation. Maximal collateral conductance was assessed with fluorescent microspheres under maximal vasodilation; cellular migration and proliferation (Ki-67) was evaluated by quantitative immunohistology.
Collateral conductance was significantly reduced by aspirin treatment, whereas clopidogrel had a neutral effect (saline: 0.94 ± 0.04; clopidogrel: 0.94 ± 0.05; aspirin: 0.64 ± 0.03 ml·min−1·100 mm Hg−1·g−1; p < 0.001). Ki-67 proliferation indexes were consistent with these results (saline: 23.1 ± 2.9%; clopidogrel: 23.5 ± 1.1%; aspirin: 19.2 ± 1.1% Ki-67–positive cells). Immunohistochemistry showed COX expression in collateral arteries and a significantly decreased monocyte/macrophage accumulation in the perivascular tissue after aspirin treatment. Cell adhesion molecule expression on monocytes after activation was significantly reduced by aspirin, which might explain the reduced migratory ability.
In summary, clopidogrel had a neutral effect on natural arteriogenesis. Aspirin significantly inhibited collateral artery growth, probably due to its anti-inflammatory effect. Additional studies are needed to substantiate these results before translation into clinical practice.</description><subject>Animals</subject><subject>Arterial Occlusive Diseases - drug therapy</subject><subject>Arterial Occlusive Diseases - physiopathology</subject><subject>Aspirin</subject><subject>Aspirin - therapeutic use</subject><subject>Blood platelets</subject><subject>Blood pressure</subject><subject>Cardiology</subject><subject>Cardiovascular disease</subject><subject>Cell adhesion & migration</subject><subject>Cytokines</subject><subject>Disease Models, Animal</subject><subject>Electrophysiology</subject><subject>Endothelium</subject><subject>Femoral Artery - drug effects</subject><subject>Femoral Artery - physiopathology</subject><subject>Laboratory animals</subject><subject>Mortality</subject><subject>Rabbits</subject><subject>Studies</subject><subject>Ticlopidine - analogs & derivatives</subject><subject>Ticlopidine - therapeutic use</subject><subject>Veins & arteries</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kVGL1DAUhYMo7rj6B3yQgODTtt4kTZuAL7ODuwqrC4s-h0xyKymdZkxaYf-9KTMg7INPuYTvHO49h5C3DGoGrP041IN1ruYAsgZeg26ekQ2TUlVC6u452UAnZMVAdxfkVc4DALSK6ZfkgrWsVVyxDRm2-RhSmK7o9TLT73GmuzEeg4-_Eo5X9AH94jDTXRxHO2OyYxmn8jfbySENE7X0we73YabfoseRxp7e4CGu4DYVwSO9d25ccojTa_Kit2PGN-f3kvy8-fxj96W6u7_9utveVa5pYa4445rpPfhOgBLaguWdF43mfeM0B-l72UqU3nWSi1YqIRqhGJOtAt7zphOX5MPJ95ji7wXzbA4hOywHTBiXbFoltezUCr5_Ag5xSVPZzTAJJaJizgvFT5RLMeeEvTmmcLDp0TAwaw9mMGsPZu3BADelhyJ6d7Ze9gf0_yTn4Avw6QRgSeJPwGSyC1gy9SGhm42P4X_-fwFooZYS</recordid><startdate>20050920</startdate><enddate>20050920</enddate><creator>Hoefer, Imo E.</creator><creator>Grundmann, Sebastian</creator><creator>Schirmer, Stephan</creator><creator>van Royen, Niels</creator><creator>Meder, Benjamin</creator><creator>Bode, Christoph</creator><creator>Piek, Jan J.</creator><creator>Buschmann, Ivo R.</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</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>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20050920</creationdate><title>Aspirin, But Not Clopidogrel, Reduces Collateral Conductance in a Rabbit Model of Femoral Artery Occlusion</title><author>Hoefer, Imo E. ; Grundmann, Sebastian ; Schirmer, Stephan ; van Royen, Niels ; Meder, Benjamin ; Bode, Christoph ; Piek, Jan J. ; Buschmann, Ivo R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c460t-212919b0d730839a0a27d3492f4c9205df565e5dc7523658334381156802f2473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Arterial Occlusive Diseases - drug therapy</topic><topic>Arterial Occlusive Diseases - physiopathology</topic><topic>Aspirin</topic><topic>Aspirin - therapeutic use</topic><topic>Blood platelets</topic><topic>Blood pressure</topic><topic>Cardiology</topic><topic>Cardiovascular disease</topic><topic>Cell adhesion & migration</topic><topic>Cytokines</topic><topic>Disease Models, Animal</topic><topic>Electrophysiology</topic><topic>Endothelium</topic><topic>Femoral Artery - drug effects</topic><topic>Femoral Artery - physiopathology</topic><topic>Laboratory animals</topic><topic>Mortality</topic><topic>Rabbits</topic><topic>Studies</topic><topic>Ticlopidine - analogs & derivatives</topic><topic>Ticlopidine - therapeutic use</topic><topic>Veins & arteries</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hoefer, Imo E.</creatorcontrib><creatorcontrib>Grundmann, Sebastian</creatorcontrib><creatorcontrib>Schirmer, Stephan</creatorcontrib><creatorcontrib>van Royen, Niels</creatorcontrib><creatorcontrib>Meder, Benjamin</creatorcontrib><creatorcontrib>Bode, Christoph</creatorcontrib><creatorcontrib>Piek, Jan J.</creatorcontrib><creatorcontrib>Buschmann, Ivo R.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of the American College of Cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hoefer, Imo E.</au><au>Grundmann, Sebastian</au><au>Schirmer, Stephan</au><au>van Royen, Niels</au><au>Meder, Benjamin</au><au>Bode, Christoph</au><au>Piek, Jan J.</au><au>Buschmann, Ivo R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aspirin, But Not Clopidogrel, Reduces Collateral Conductance in a Rabbit Model of Femoral Artery Occlusion</atitle><jtitle>Journal of the American College of Cardiology</jtitle><addtitle>J Am Coll Cardiol</addtitle><date>2005-09-20</date><risdate>2005</risdate><volume>46</volume><issue>6</issue><spage>994</spage><epage>1001</epage><pages>994-1001</pages><issn>0735-1097</issn><eissn>1558-3597</eissn><abstract>The objective of this study was to test the potential of aspirin and clopidogrel to influence collateral artery growth (arteriogenesis).
Aspirin and clopidogrel are antiplatelet agents commonly used in the treatment of ischemic cardiovascular disease. Both inhibit platelet aggregation; however, they differ mechanistically because aspirin acts via cyclooxygenase (COX) inhibition, while clopidogrel noncompetitively antagonizes the P2Y12adenosine diphosphate receptor. We hypothesized that aspirin, due to its anti-inflammatory effects through inhibition of COX activity could inhibit arteriogenesis. Given that clopidogrel does not affect COX activity, it would be less likely to interfere with collateral artery growth.
Fifty-four New Zealand White rabbits received either saline, aspirin (10 mg/kg), or clopidogrel (10 mg/kg) for seven days after femoral artery ligation. Maximal collateral conductance was assessed with fluorescent microspheres under maximal vasodilation; cellular migration and proliferation (Ki-67) was evaluated by quantitative immunohistology.
Collateral conductance was significantly reduced by aspirin treatment, whereas clopidogrel had a neutral effect (saline: 0.94 ± 0.04; clopidogrel: 0.94 ± 0.05; aspirin: 0.64 ± 0.03 ml·min−1·100 mm Hg−1·g−1; p < 0.001). Ki-67 proliferation indexes were consistent with these results (saline: 23.1 ± 2.9%; clopidogrel: 23.5 ± 1.1%; aspirin: 19.2 ± 1.1% Ki-67–positive cells). Immunohistochemistry showed COX expression in collateral arteries and a significantly decreased monocyte/macrophage accumulation in the perivascular tissue after aspirin treatment. Cell adhesion molecule expression on monocytes after activation was significantly reduced by aspirin, which might explain the reduced migratory ability.
In summary, clopidogrel had a neutral effect on natural arteriogenesis. Aspirin significantly inhibited collateral artery growth, probably due to its anti-inflammatory effect. Additional studies are needed to substantiate these results before translation into clinical practice.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>16168281</pmid><doi>10.1016/j.jacc.2005.02.094</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Arterial Occlusive Diseases - drug therapy Arterial Occlusive Diseases - physiopathology Aspirin Aspirin - therapeutic use Blood platelets Blood pressure Cardiology Cardiovascular disease Cell adhesion & migration Cytokines Disease Models, Animal Electrophysiology Endothelium Femoral Artery - drug effects Femoral Artery - physiopathology Laboratory animals Mortality Rabbits Studies Ticlopidine - analogs & derivatives Ticlopidine - therapeutic use Veins & arteries |
| title | Aspirin, But Not Clopidogrel, Reduces Collateral Conductance in a Rabbit Model of Femoral Artery Occlusion |
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