ELEVATED CONCENTRATIONS OF ENDOGENOUS OUABAIN IN PATIENTS WITH CONGESTIVE-HEART-FAILURE

Background. An endogenous digitalis-like compound in mammals has long been postulated, but only recently has a substance indistinguishable from ouabain been identified in human plasma. Because of the potential significance of such a substance in patients with congestive heart failure, we sought to e...

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Veröffentlicht in:Circulation (New York, N.Y.) N.Y.), 1992-08, Vol.86 (2), p.420-425
Hauptverfasser: GOTTLIEB, SS, ROGOWSKI, AC, WEINBERG, M, KRICHTEN, CM, HAMILTON, BP, HAMLYN, JM
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container_end_page 425
container_issue 2
container_start_page 420
container_title Circulation (New York, N.Y.)
container_volume 86
creator GOTTLIEB, SS
ROGOWSKI, AC
WEINBERG, M
KRICHTEN, CM
HAMILTON, BP
HAMLYN, JM
description Background. An endogenous digitalis-like compound in mammals has long been postulated, but only recently has a substance indistinguishable from ouabain been identified in human plasma. Because of the potential significance of such a substance in patients with congestive heart failure, we sought to evaluate the pathophysiology of endogenous ouabain in these individuals. Methods and Results. Using an immunoassay, we determined plasma ouabain concentrations in 51 patients with heart failure and in 19 control subjects. Plasma ouabain concentrations in control subjects ranged from 0.16 to 0.77 nM (mean, 0.44+/-0.20 nM). In 19 matched heart failure patients receiving digoxin, the mean ouabain was significantly elevated at 1.59+/-2.2 nM (range, 0.17-8.76 nM, p
doi_str_mv 10.1161/01.CIR.86.2.420
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An endogenous digitalis-like compound in mammals has long been postulated, but only recently has a substance indistinguishable from ouabain been identified in human plasma. Because of the potential significance of such a substance in patients with congestive heart failure, we sought to evaluate the pathophysiology of endogenous ouabain in these individuals. Methods and Results. Using an immunoassay, we determined plasma ouabain concentrations in 51 patients with heart failure and in 19 control subjects. Plasma ouabain concentrations in control subjects ranged from 0.16 to 0.77 nM (mean, 0.44+/-0.20 nM). In 19 matched heart failure patients receiving digoxin, the mean ouabain was significantly elevated at 1.59+/-2.2 nM (range, 0.17-8.76 nM, p&lt;0.05 versus control subjects). The ouabain concentration correlated inversely with both cardiac index (r=-0.62, p&lt;0.005) and mean arterial pressure (r=-0.51, p&lt;0.05). However, there was no correlation between ouabain and left ventricular filling (r=0.19, NS) or right atrial pressures (r=0.20, NS). In 16 heart failure patients not receiving digoxin, the mean ouabain was 1.52+/-2.58 nM. No relation between renal function and ouabain was detected. Conclusions. The unanticipated lack of correlation of ouabain with atrial pressures indicates that volume is not the chief determinant of ouabain concentration in patients with congestive heart failure. However, the significant relations of plasma ouabain concentration with cardiac index and mean arterial pressure imply that endogenous ouabain may be an important homeostatic factor in humans.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.86.2.420</identifier><identifier>PMID: 1322253</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>DALLAS: Amer Heart Assoc</publisher><subject>Biological and medical sciences ; Cardiac &amp; Cardiovascular Systems ; Cardiology. Vascular system ; Cardiovascular System &amp; Cardiology ; Digoxin - therapeutic use ; Female ; Glomerular Filtration Rate ; Heart ; Heart Failure - blood ; Heart Failure - drug therapy ; Heart Failure - physiopathology ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Hemodynamics - physiology ; Homeostasis - physiology ; Humans ; Immunoassay ; Life Sciences &amp; Biomedicine ; Male ; Medical sciences ; Middle Aged ; Ouabain - blood ; Peripheral Vascular Disease ; Science &amp; Technology ; Sodium-Potassium-Exchanging ATPase - antagonists &amp; inhibitors</subject><ispartof>Circulation (New York, N.Y.), 1992-08, Vol.86 (2), p.420-425</ispartof><rights>1992 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>192</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wosA1992JH00900009</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c448t-10273e062b68b95d216f5d78cacbc8c50775857f2fb9a42f58a4d896bdc22c163</citedby><cites>FETCH-LOGICAL-c448t-10273e062b68b95d216f5d78cacbc8c50775857f2fb9a42f58a4d896bdc22c163</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,3688,27197,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=5523867$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1322253$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GOTTLIEB, SS</creatorcontrib><creatorcontrib>ROGOWSKI, AC</creatorcontrib><creatorcontrib>WEINBERG, M</creatorcontrib><creatorcontrib>KRICHTEN, CM</creatorcontrib><creatorcontrib>HAMILTON, BP</creatorcontrib><creatorcontrib>HAMLYN, JM</creatorcontrib><title>ELEVATED CONCENTRATIONS OF ENDOGENOUS OUABAIN IN PATIENTS WITH CONGESTIVE-HEART-FAILURE</title><title>Circulation (New York, N.Y.)</title><addtitle>CIRCULATION</addtitle><addtitle>Circulation</addtitle><description>Background. An endogenous digitalis-like compound in mammals has long been postulated, but only recently has a substance indistinguishable from ouabain been identified in human plasma. Because of the potential significance of such a substance in patients with congestive heart failure, we sought to evaluate the pathophysiology of endogenous ouabain in these individuals. Methods and Results. Using an immunoassay, we determined plasma ouabain concentrations in 51 patients with heart failure and in 19 control subjects. Plasma ouabain concentrations in control subjects ranged from 0.16 to 0.77 nM (mean, 0.44+/-0.20 nM). In 19 matched heart failure patients receiving digoxin, the mean ouabain was significantly elevated at 1.59+/-2.2 nM (range, 0.17-8.76 nM, p&lt;0.05 versus control subjects). The ouabain concentration correlated inversely with both cardiac index (r=-0.62, p&lt;0.005) and mean arterial pressure (r=-0.51, p&lt;0.05). However, there was no correlation between ouabain and left ventricular filling (r=0.19, NS) or right atrial pressures (r=0.20, NS). In 16 heart failure patients not receiving digoxin, the mean ouabain was 1.52+/-2.58 nM. No relation between renal function and ouabain was detected. Conclusions. The unanticipated lack of correlation of ouabain with atrial pressures indicates that volume is not the chief determinant of ouabain concentration in patients with congestive heart failure. However, the significant relations of plasma ouabain concentration with cardiac index and mean arterial pressure imply that endogenous ouabain may be an important homeostatic factor in humans.</description><subject>Biological and medical sciences</subject><subject>Cardiac &amp; Cardiovascular Systems</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular System &amp; Cardiology</subject><subject>Digoxin - therapeutic use</subject><subject>Female</subject><subject>Glomerular Filtration Rate</subject><subject>Heart</subject><subject>Heart Failure - blood</subject><subject>Heart Failure - drug therapy</subject><subject>Heart Failure - physiopathology</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>Hemodynamics - physiology</subject><subject>Homeostasis - physiology</subject><subject>Humans</subject><subject>Immunoassay</subject><subject>Life Sciences &amp; Biomedicine</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Ouabain - blood</subject><subject>Peripheral Vascular Disease</subject><subject>Science &amp; Technology</subject><subject>Sodium-Potassium-Exchanging ATPase - antagonists &amp; inhibitors</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EZCTM</sourceid><sourceid>EIF</sourceid><recordid>eNqN0c9r2zAUB3AxOro023mngQ9ll2FXP6wfPrqukngEeyROexSyLINHYreWw9h_X4WE7DoQCOl93jt8HwBfEYwQYugBoijLN5FgEY5iDD-AGaI4DmNKkhswgxAmIScYfwJ3zv32T0Y4vQW3yP9hSmbgRa7lc1rJpyAri0wW1Sat8rLYBuUikMVTuZRFufOvXfqY5kXgzy8PvNsGL3m1OnUt5bbKn2W4kummChdpvt5t5GfwsdV7Z79c7jnYLWSVrcJ1ucyzdB2aOBZTiCDmxEKGaybqhDYYsZY2XBhtaiMMhZxTQXmL2zrRMW6p0HEjElY3BmODGJmD7-e5r-PwdrRuUofOGbvf694OR6c4gQmh8Qk-nKEZB-dG26rXsTvo8a9CUJ2iVBApH6USTGHlo_Qd3y6jj_XBNv_8OTtfv7_UtTN63466N527MkoxEYx79uPM_th6aJ3pbG_sVaUoSfDPld8TPC3La_H_OusmPXVDnw3HfiLvEHaUPw</recordid><startdate>19920801</startdate><enddate>19920801</enddate><creator>GOTTLIEB, SS</creator><creator>ROGOWSKI, AC</creator><creator>WEINBERG, M</creator><creator>KRICHTEN, CM</creator><creator>HAMILTON, BP</creator><creator>HAMLYN, JM</creator><general>Amer Heart Assoc</general><general>Lippincott Williams &amp; Wilkins</general><scope>BLEPL</scope><scope>DTL</scope><scope>EZCTM</scope><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>7X8</scope></search><sort><creationdate>19920801</creationdate><title>ELEVATED CONCENTRATIONS OF ENDOGENOUS OUABAIN IN PATIENTS WITH CONGESTIVE-HEART-FAILURE</title><author>GOTTLIEB, SS ; ROGOWSKI, AC ; WEINBERG, M ; KRICHTEN, CM ; HAMILTON, BP ; HAMLYN, JM</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-10273e062b68b95d216f5d78cacbc8c50775857f2fb9a42f58a4d896bdc22c163</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Biological and medical sciences</topic><topic>Cardiac &amp; Cardiovascular Systems</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular System &amp; Cardiology</topic><topic>Digoxin - therapeutic use</topic><topic>Female</topic><topic>Glomerular Filtration Rate</topic><topic>Heart</topic><topic>Heart Failure - blood</topic><topic>Heart Failure - drug therapy</topic><topic>Heart Failure - physiopathology</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>Hemodynamics - physiology</topic><topic>Homeostasis - physiology</topic><topic>Humans</topic><topic>Immunoassay</topic><topic>Life Sciences &amp; Biomedicine</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Ouabain - blood</topic><topic>Peripheral Vascular Disease</topic><topic>Science &amp; Technology</topic><topic>Sodium-Potassium-Exchanging ATPase - antagonists &amp; inhibitors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GOTTLIEB, SS</creatorcontrib><creatorcontrib>ROGOWSKI, AC</creatorcontrib><creatorcontrib>WEINBERG, M</creatorcontrib><creatorcontrib>KRICHTEN, CM</creatorcontrib><creatorcontrib>HAMILTON, BP</creatorcontrib><creatorcontrib>HAMLYN, JM</creatorcontrib><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Web of Science - Science Citation Index Expanded - 1992</collection><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>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GOTTLIEB, SS</au><au>ROGOWSKI, AC</au><au>WEINBERG, M</au><au>KRICHTEN, CM</au><au>HAMILTON, BP</au><au>HAMLYN, JM</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ELEVATED CONCENTRATIONS OF ENDOGENOUS OUABAIN IN PATIENTS WITH CONGESTIVE-HEART-FAILURE</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><stitle>CIRCULATION</stitle><addtitle>Circulation</addtitle><date>1992-08-01</date><risdate>1992</risdate><volume>86</volume><issue>2</issue><spage>420</spage><epage>425</epage><pages>420-425</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Background. An endogenous digitalis-like compound in mammals has long been postulated, but only recently has a substance indistinguishable from ouabain been identified in human plasma. Because of the potential significance of such a substance in patients with congestive heart failure, we sought to evaluate the pathophysiology of endogenous ouabain in these individuals. Methods and Results. Using an immunoassay, we determined plasma ouabain concentrations in 51 patients with heart failure and in 19 control subjects. Plasma ouabain concentrations in control subjects ranged from 0.16 to 0.77 nM (mean, 0.44+/-0.20 nM). In 19 matched heart failure patients receiving digoxin, the mean ouabain was significantly elevated at 1.59+/-2.2 nM (range, 0.17-8.76 nM, p&lt;0.05 versus control subjects). The ouabain concentration correlated inversely with both cardiac index (r=-0.62, p&lt;0.005) and mean arterial pressure (r=-0.51, p&lt;0.05). However, there was no correlation between ouabain and left ventricular filling (r=0.19, NS) or right atrial pressures (r=0.20, NS). In 16 heart failure patients not receiving digoxin, the mean ouabain was 1.52+/-2.58 nM. No relation between renal function and ouabain was detected. Conclusions. The unanticipated lack of correlation of ouabain with atrial pressures indicates that volume is not the chief determinant of ouabain concentration in patients with congestive heart failure. However, the significant relations of plasma ouabain concentration with cardiac index and mean arterial pressure imply that endogenous ouabain may be an important homeostatic factor in humans.</abstract><cop>DALLAS</cop><pub>Amer Heart Assoc</pub><pmid>1322253</pmid><doi>10.1161/01.CIR.86.2.420</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record>
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source Web of Science - Science Citation Index Expanded - 1992<img src="https://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" />; MEDLINE; American Heart Association Journals; Journals@Ovid Ovid Autoload; EZB-FREE-00999 freely available EZB journals
subjects Biological and medical sciences
Cardiac & Cardiovascular Systems
Cardiology. Vascular system
Cardiovascular System & Cardiology
Digoxin - therapeutic use
Female
Glomerular Filtration Rate
Heart
Heart Failure - blood
Heart Failure - drug therapy
Heart Failure - physiopathology
Heart failure, cardiogenic pulmonary edema, cardiac enlargement
Hemodynamics - physiology
Homeostasis - physiology
Humans
Immunoassay
Life Sciences & Biomedicine
Male
Medical sciences
Middle Aged
Ouabain - blood
Peripheral Vascular Disease
Science & Technology
Sodium-Potassium-Exchanging ATPase - antagonists & inhibitors
title ELEVATED CONCENTRATIONS OF ENDOGENOUS OUABAIN IN PATIENTS WITH CONGESTIVE-HEART-FAILURE
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