Allopurinol improves endothelial dysfunction in chronic Heart failure
Increased oxidative stress in chronic heart failure is thought to contribute to endothelial dysfunction. Xanthine oxidase produces oxidative stress and therefore we examined whether allopurinol improved endothelial dysfunction in chronic heart failure. We performed a randomized, placebo-controlled,...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2002-07, Vol.106 (2), p.221-226 |
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| container_title | Circulation (New York, N.Y.) |
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| creator | FARQUHARSON, Colin A. J BUTLER, Robert HILL, Alexander BELCH, Jill J. F STRUTHERS, Allan D |
| description | Increased oxidative stress in chronic heart failure is thought to contribute to endothelial dysfunction. Xanthine oxidase produces oxidative stress and therefore we examined whether allopurinol improved endothelial dysfunction in chronic heart failure.
We performed a randomized, placebo-controlled, double-blind crossover study on 11 patients with New York Heart Association class II-III chronic heart failure, comparing 300 mg allopurinol daily (1 month) versus placebo. Endothelial function was assessed by standard forearm venous occlusion plethysmography with acetylcholine, nitroprusside, and verapamil. Plasma malondialdehyde levels were also compared to assess significant changes in oxidative stress. Allopurinol significantly increased the forearm blood flow response to acetylcholine (percentage change in forearm blood flow [mean+/-SEM]: 181+/-19% versus 120+/-22% allopurinol versus placebo; P=0.003). There were no significant differences in the forearm blood flow changes between the placebo and allopurinol treatment arms with regard to sodium nitroprusside or verapamil. Plasma malondialdehyde was significantly reduced with allopurinol treatment (346+/-128 nmol/L versus 461+/-101 nmol/L, allopurinol versus placebo; P=0.03), consistent with reduced oxidative stress with allopurinol therapy.
We have shown that allopurinol improves endothelial dysfunction in chronic heart failure. This raises the distinct possibility that allopurinol might reduce cardiovascular events and even improve exercise capacity in chronic heart failure. |
| doi_str_mv | 10.1161/01.CIR.0000022140.61460.1D |
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We performed a randomized, placebo-controlled, double-blind crossover study on 11 patients with New York Heart Association class II-III chronic heart failure, comparing 300 mg allopurinol daily (1 month) versus placebo. Endothelial function was assessed by standard forearm venous occlusion plethysmography with acetylcholine, nitroprusside, and verapamil. Plasma malondialdehyde levels were also compared to assess significant changes in oxidative stress. Allopurinol significantly increased the forearm blood flow response to acetylcholine (percentage change in forearm blood flow [mean+/-SEM]: 181+/-19% versus 120+/-22% allopurinol versus placebo; P=0.003). There were no significant differences in the forearm blood flow changes between the placebo and allopurinol treatment arms with regard to sodium nitroprusside or verapamil. Plasma malondialdehyde was significantly reduced with allopurinol treatment (346+/-128 nmol/L versus 461+/-101 nmol/L, allopurinol versus placebo; P=0.03), consistent with reduced oxidative stress with allopurinol therapy.
We have shown that allopurinol improves endothelial dysfunction in chronic heart failure. This raises the distinct possibility that allopurinol might reduce cardiovascular events and even improve exercise capacity in chronic heart failure.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.0000022140.61460.1D</identifier><identifier>PMID: 12105162</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Aged ; Allopurinol - therapeutic use ; Antioxidants - therapeutic use ; Biological and medical sciences ; Blood Pressure - drug effects ; Chronic Disease ; Cross-Over Studies ; Double-Blind Method ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - physiopathology ; Enzyme Inhibitors - therapeutic use ; Female ; Forearm - blood supply ; General and cellular metabolism. Vitamins ; Heart Failure - blood ; Heart Failure - drug therapy ; Heart Failure - physiopathology ; Heart Rate - drug effects ; Humans ; Male ; Malondialdehyde - blood ; Medical sciences ; Pharmacology. Drug treatments ; Regional Blood Flow - drug effects ; Vasodilator Agents - pharmacology ; Xanthine Oxidase - antagonists & inhibitors</subject><ispartof>Circulation (New York, N.Y.), 2002-07, Vol.106 (2), p.221-226</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Jul 9, 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c588t-c5ca352e910a520e58fdfaa8bbde3157656c162411f2c363943fd7e3d1e35d6f3</citedby><cites>FETCH-LOGICAL-c588t-c5ca352e910a520e58fdfaa8bbde3157656c162411f2c363943fd7e3d1e35d6f3</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=13791314$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12105162$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FARQUHARSON, Colin A. J</creatorcontrib><creatorcontrib>BUTLER, Robert</creatorcontrib><creatorcontrib>HILL, Alexander</creatorcontrib><creatorcontrib>BELCH, Jill J. F</creatorcontrib><creatorcontrib>STRUTHERS, Allan D</creatorcontrib><title>Allopurinol improves endothelial dysfunction in chronic Heart failure</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Increased oxidative stress in chronic heart failure is thought to contribute to endothelial dysfunction. Xanthine oxidase produces oxidative stress and therefore we examined whether allopurinol improved endothelial dysfunction in chronic heart failure.
We performed a randomized, placebo-controlled, double-blind crossover study on 11 patients with New York Heart Association class II-III chronic heart failure, comparing 300 mg allopurinol daily (1 month) versus placebo. Endothelial function was assessed by standard forearm venous occlusion plethysmography with acetylcholine, nitroprusside, and verapamil. Plasma malondialdehyde levels were also compared to assess significant changes in oxidative stress. Allopurinol significantly increased the forearm blood flow response to acetylcholine (percentage change in forearm blood flow [mean+/-SEM]: 181+/-19% versus 120+/-22% allopurinol versus placebo; P=0.003). There were no significant differences in the forearm blood flow changes between the placebo and allopurinol treatment arms with regard to sodium nitroprusside or verapamil. Plasma malondialdehyde was significantly reduced with allopurinol treatment (346+/-128 nmol/L versus 461+/-101 nmol/L, allopurinol versus placebo; P=0.03), consistent with reduced oxidative stress with allopurinol therapy.
We have shown that allopurinol improves endothelial dysfunction in chronic heart failure. This raises the distinct possibility that allopurinol might reduce cardiovascular events and even improve exercise capacity in chronic heart failure.</description><subject>Aged</subject><subject>Allopurinol - therapeutic use</subject><subject>Antioxidants - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Chronic Disease</subject><subject>Cross-Over Studies</subject><subject>Double-Blind Method</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Enzyme Inhibitors - therapeutic use</subject><subject>Female</subject><subject>Forearm - blood supply</subject><subject>General and cellular metabolism. Vitamins</subject><subject>Heart Failure - blood</subject><subject>Heart Failure - drug therapy</subject><subject>Heart Failure - physiopathology</subject><subject>Heart Rate - drug effects</subject><subject>Humans</subject><subject>Male</subject><subject>Malondialdehyde - blood</subject><subject>Medical sciences</subject><subject>Pharmacology. Drug treatments</subject><subject>Regional Blood Flow - drug effects</subject><subject>Vasodilator Agents - pharmacology</subject><subject>Xanthine Oxidase - antagonists & inhibitors</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkF1LwzAUhoMoOqd_QYqgd6s5SZO23sn82GAgiF6HLE0wkiYzaYX9e6MOBubihMN5TvLyIHQJuATgcIOhnC9fSvxzCIEKlxwqnof3B2gCjFSzitH2EE3yvJ3VlJATdJrSR245rdkxOgECmAEnE_Rw51zYjNH64Arbb2L40qnQvgvDu3ZWuqLbJjN6NdjgC-sL9R6Dt6pYaBmHwkjrxqjP0JGRLunz3T1Fb48Pr_PFbPX8tJzfrWaKNc2Qq5KUEd0CloxgzRrTGSmb9brTFFjNGVc5VQVgiKKcthU1Xa1pB5qyjhs6Rdd_7-acn6NOg-htUto56XUYk6ihaWrCIIOX_8CPMEafswkChDfQ4ipDt3-QiiGlqI3YRNvLuBWAxY9pgUFk02JvWvyaFnCfly92P4zrXnf71Z3aDFztAJmUdCZKr2zac7RugUJFvwFtqoZ8</recordid><startdate>20020709</startdate><enddate>20020709</enddate><creator>FARQUHARSON, Colin A. J</creator><creator>BUTLER, Robert</creator><creator>HILL, Alexander</creator><creator>BELCH, Jill J. F</creator><creator>STRUTHERS, Allan D</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>20020709</creationdate><title>Allopurinol improves endothelial dysfunction in chronic Heart failure</title><author>FARQUHARSON, Colin A. J ; BUTLER, Robert ; HILL, Alexander ; BELCH, Jill J. F ; STRUTHERS, Allan D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c588t-c5ca352e910a520e58fdfaa8bbde3157656c162411f2c363943fd7e3d1e35d6f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Aged</topic><topic>Allopurinol - therapeutic use</topic><topic>Antioxidants - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Chronic Disease</topic><topic>Cross-Over Studies</topic><topic>Double-Blind Method</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Enzyme Inhibitors - therapeutic use</topic><topic>Female</topic><topic>Forearm - blood supply</topic><topic>General and cellular metabolism. Vitamins</topic><topic>Heart Failure - blood</topic><topic>Heart Failure - drug therapy</topic><topic>Heart Failure - physiopathology</topic><topic>Heart Rate - drug effects</topic><topic>Humans</topic><topic>Male</topic><topic>Malondialdehyde - blood</topic><topic>Medical sciences</topic><topic>Pharmacology. Drug treatments</topic><topic>Regional Blood Flow - drug effects</topic><topic>Vasodilator Agents - pharmacology</topic><topic>Xanthine Oxidase - antagonists & inhibitors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FARQUHARSON, Colin A. J</creatorcontrib><creatorcontrib>BUTLER, Robert</creatorcontrib><creatorcontrib>HILL, Alexander</creatorcontrib><creatorcontrib>BELCH, Jill J. F</creatorcontrib><creatorcontrib>STRUTHERS, Allan D</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>FARQUHARSON, Colin A. J</au><au>BUTLER, Robert</au><au>HILL, Alexander</au><au>BELCH, Jill J. F</au><au>STRUTHERS, Allan D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Allopurinol improves endothelial dysfunction in chronic Heart failure</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2002-07-09</date><risdate>2002</risdate><volume>106</volume><issue>2</issue><spage>221</spage><epage>226</epage><pages>221-226</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Increased oxidative stress in chronic heart failure is thought to contribute to endothelial dysfunction. Xanthine oxidase produces oxidative stress and therefore we examined whether allopurinol improved endothelial dysfunction in chronic heart failure.
We performed a randomized, placebo-controlled, double-blind crossover study on 11 patients with New York Heart Association class II-III chronic heart failure, comparing 300 mg allopurinol daily (1 month) versus placebo. Endothelial function was assessed by standard forearm venous occlusion plethysmography with acetylcholine, nitroprusside, and verapamil. Plasma malondialdehyde levels were also compared to assess significant changes in oxidative stress. Allopurinol significantly increased the forearm blood flow response to acetylcholine (percentage change in forearm blood flow [mean+/-SEM]: 181+/-19% versus 120+/-22% allopurinol versus placebo; P=0.003). There were no significant differences in the forearm blood flow changes between the placebo and allopurinol treatment arms with regard to sodium nitroprusside or verapamil. Plasma malondialdehyde was significantly reduced with allopurinol treatment (346+/-128 nmol/L versus 461+/-101 nmol/L, allopurinol versus placebo; P=0.03), consistent with reduced oxidative stress with allopurinol therapy.
We have shown that allopurinol improves endothelial dysfunction in chronic heart failure. This raises the distinct possibility that allopurinol might reduce cardiovascular events and even improve exercise capacity in chronic heart failure.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>12105162</pmid><doi>10.1161/01.CIR.0000022140.61460.1D</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | Journals@Ovid Ovid Autoload; MEDLINE; American Heart Association Journals; EZB-FREE-00999 freely available EZB journals |
| subjects | Aged Allopurinol - therapeutic use Antioxidants - therapeutic use Biological and medical sciences Blood Pressure - drug effects Chronic Disease Cross-Over Studies Double-Blind Method Endothelium, Vascular - drug effects Endothelium, Vascular - physiopathology Enzyme Inhibitors - therapeutic use Female Forearm - blood supply General and cellular metabolism. Vitamins Heart Failure - blood Heart Failure - drug therapy Heart Failure - physiopathology Heart Rate - drug effects Humans Male Malondialdehyde - blood Medical sciences Pharmacology. Drug treatments Regional Blood Flow - drug effects Vasodilator Agents - pharmacology Xanthine Oxidase - antagonists & inhibitors |
| title | Allopurinol improves endothelial dysfunction in chronic Heart failure |
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