Selective contractile dysfunction of left, not right, ventricular myocardium in the SHHF rat
1 Institute of Molecular Cardiobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205; and 2 Department of Physiology and Cell Biology and 3 Dorothy M. Davis Heart and Lung Institute, Ohio State University, Columbus, Ohio 43210 The progression of hypertension to cardiac f...
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| Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2003-03, Vol.284 (3), p.H772-H778 |
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| container_title | American journal of physiology. Heart and circulatory physiology |
| container_volume | 284 |
| creator | Janssen, Paul M. L Stull, Linda B Leppo, Michelle K Altschuld, Ruth A Marban, Eduardo |
| description | 1 Institute of Molecular Cardiobiology, Johns
Hopkins University School of Medicine, Baltimore, Maryland 21205;
and 2 Department of Physiology and Cell Biology and
3 Dorothy M. Davis Heart and Lung Institute, Ohio
State University, Columbus, Ohio 43210
The progression of hypertension to
cardiac failure involves systemic changes that may ultimately affect
contractility throughout the heart. Spontaneous hypertensive heart
failure (SHHF) rats have depressed left ventricular (LV) function, but
right ventricular (RV) dysfunction is less well characterized.
Ultrathin (87 ± 5 µm) trabeculae were isolated from end-stage
failing SHHF rats and from age-matched controls. Under
near-physiological conditions (1 mM Ca 2+ , 37°C, 4 Hz),
developed force (in mN/mm 2 ) was not significantly different
in SHHF LV and RV trabeculae and those of controls. SHHF LV
preparations displayed a negative force-frequency behavior (40 ± 7 vs. 23 ± 4 mN/mm 2 , 2 vs. 7 Hz); this relationship
was positive in SHHF RV preparations (27 ± 5 vs. 40 ± 6 mN/mm 2 ) and controls (32 ± 6 vs. 44 ± 9 mN/mm 2 ). The response to isoproterenol (10 6
M, 4 Hz) was depressed in SHHF LV preparations. The inotropic response
to hypothermia was lost in SHHF LV trabeculae but preserved in SHHF RV
trabeculae. Intracellular calcium measurements revealed impaired
calcium handling at higher frequencies in LV preparations. We conclude
that in end-stage failing SHHF rats, RV function is only marginally
affected, whereas a severe contractile dysfunction of LV myocardium is present.
contractile function; excitation-contraction coupling; heart
failure; inotropic agents; hypertension |
| doi_str_mv | 10.1152/ajpheart.01061.2001 |
| format | Article |
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Hopkins University School of Medicine, Baltimore, Maryland 21205;
and 2 Department of Physiology and Cell Biology and
3 Dorothy M. Davis Heart and Lung Institute, Ohio
State University, Columbus, Ohio 43210
The progression of hypertension to
cardiac failure involves systemic changes that may ultimately affect
contractility throughout the heart. Spontaneous hypertensive heart
failure (SHHF) rats have depressed left ventricular (LV) function, but
right ventricular (RV) dysfunction is less well characterized.
Ultrathin (87 ± 5 µm) trabeculae were isolated from end-stage
failing SHHF rats and from age-matched controls. Under
near-physiological conditions (1 mM Ca 2+ , 37°C, 4 Hz),
developed force (in mN/mm 2 ) was not significantly different
in SHHF LV and RV trabeculae and those of controls. SHHF LV
preparations displayed a negative force-frequency behavior (40 ± 7 vs. 23 ± 4 mN/mm 2 , 2 vs. 7 Hz); this relationship
was positive in SHHF RV preparations (27 ± 5 vs. 40 ± 6 mN/mm 2 ) and controls (32 ± 6 vs. 44 ± 9 mN/mm 2 ). The response to isoproterenol (10 6
M, 4 Hz) was depressed in SHHF LV preparations. The inotropic response
to hypothermia was lost in SHHF LV trabeculae but preserved in SHHF RV
trabeculae. Intracellular calcium measurements revealed impaired
calcium handling at higher frequencies in LV preparations. We conclude
that in end-stage failing SHHF rats, RV function is only marginally
affected, whereas a severe contractile dysfunction of LV myocardium is present.
contractile function; excitation-contraction coupling; heart
failure; inotropic agents; hypertension</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.01061.2001</identifier><identifier>PMID: 12424099</identifier><language>eng</language><publisher>United States</publisher><subject>Adrenergic beta-Agonists - pharmacology ; Animals ; Calcium - metabolism ; Disease Models, Animal ; Heart Failure - complications ; Heart Failure - physiopathology ; Heart Ventricles - drug effects ; Heart Ventricles - physiopathology ; Hypertension - complications ; In Vitro Techniques ; Male ; Myocardial Contraction - drug effects ; Myocardium - metabolism ; Perfusion ; Rats ; Rats, Inbred Strains ; Stress, Mechanical ; Temperature ; Ventricular Dysfunction, Left - physiopathology ; Ventricular Function, Right - drug effects</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2003-03, Vol.284 (3), p.H772-H778</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-dab706c0aa74affabd0b727efc54d17ed9a0e35688feda9d52ab25588bd0ce533</citedby><cites>FETCH-LOGICAL-c391t-dab706c0aa74affabd0b727efc54d17ed9a0e35688feda9d52ab25588bd0ce533</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3026,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12424099$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Janssen, Paul M. L</creatorcontrib><creatorcontrib>Stull, Linda B</creatorcontrib><creatorcontrib>Leppo, Michelle K</creatorcontrib><creatorcontrib>Altschuld, Ruth A</creatorcontrib><creatorcontrib>Marban, Eduardo</creatorcontrib><title>Selective contractile dysfunction of left, not right, ventricular myocardium in the SHHF rat</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>1 Institute of Molecular Cardiobiology, Johns
Hopkins University School of Medicine, Baltimore, Maryland 21205;
and 2 Department of Physiology and Cell Biology and
3 Dorothy M. Davis Heart and Lung Institute, Ohio
State University, Columbus, Ohio 43210
The progression of hypertension to
cardiac failure involves systemic changes that may ultimately affect
contractility throughout the heart. Spontaneous hypertensive heart
failure (SHHF) rats have depressed left ventricular (LV) function, but
right ventricular (RV) dysfunction is less well characterized.
Ultrathin (87 ± 5 µm) trabeculae were isolated from end-stage
failing SHHF rats and from age-matched controls. Under
near-physiological conditions (1 mM Ca 2+ , 37°C, 4 Hz),
developed force (in mN/mm 2 ) was not significantly different
in SHHF LV and RV trabeculae and those of controls. SHHF LV
preparations displayed a negative force-frequency behavior (40 ± 7 vs. 23 ± 4 mN/mm 2 , 2 vs. 7 Hz); this relationship
was positive in SHHF RV preparations (27 ± 5 vs. 40 ± 6 mN/mm 2 ) and controls (32 ± 6 vs. 44 ± 9 mN/mm 2 ). The response to isoproterenol (10 6
M, 4 Hz) was depressed in SHHF LV preparations. The inotropic response
to hypothermia was lost in SHHF LV trabeculae but preserved in SHHF RV
trabeculae. Intracellular calcium measurements revealed impaired
calcium handling at higher frequencies in LV preparations. We conclude
that in end-stage failing SHHF rats, RV function is only marginally
affected, whereas a severe contractile dysfunction of LV myocardium is present.
contractile function; excitation-contraction coupling; heart
failure; inotropic agents; hypertension</description><subject>Adrenergic beta-Agonists - pharmacology</subject><subject>Animals</subject><subject>Calcium - metabolism</subject><subject>Disease Models, Animal</subject><subject>Heart Failure - complications</subject><subject>Heart Failure - physiopathology</subject><subject>Heart Ventricles - drug effects</subject><subject>Heart Ventricles - physiopathology</subject><subject>Hypertension - complications</subject><subject>In Vitro Techniques</subject><subject>Male</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocardium - metabolism</subject><subject>Perfusion</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Stress, Mechanical</subject><subject>Temperature</subject><subject>Ventricular Dysfunction, Left - physiopathology</subject><subject>Ventricular Function, Right - drug effects</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kM1u1DAURi0EokPhCZCQV6zI4J84TtihimGQKrFo2SFZjn3dpHLiwXYKeXtcZmBWrPxJPucuDkKvKdlSKth7fX8YQMe8JZQ0dMsIoU_QpvywigrePUUbwhteNZSLC_QipXtCiJANf44uKKtZTbpug77fgAeTxwfAJsw56rI9YLsmt8xlhxkHhz24_A7PIeM43g1lPkBhR7N4HfG0BqOjHZcJjzPOA-Cb_X6Ho84v0TOnfYJXp_cSfdt9ur3aV9dfP3-5-nhdGd7RXFndS9IYorWstXO6t6SXTIIzorZUgu00AS6atnVgdWcF0z0Tom0LaEBwfoneHu8eYvixQMpqGpMB7_UMYUlKcsLqVrYF5EfQxJBSBKcOcZx0XBUl6jGq-htV_YmqHqMW683p_NJPYM_OqWIBtkdgKHV-jhHUYVjTGHy4W88XWVsrrvZSsiJ8-L-wW7y_hV_5n3kW1cE6_huP7Zzs</recordid><startdate>20030301</startdate><enddate>20030301</enddate><creator>Janssen, Paul M. L</creator><creator>Stull, Linda B</creator><creator>Leppo, Michelle K</creator><creator>Altschuld, Ruth A</creator><creator>Marban, Eduardo</creator><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>20030301</creationdate><title>Selective contractile dysfunction of left, not right, ventricular myocardium in the SHHF rat</title><author>Janssen, Paul M. L ; Stull, Linda B ; Leppo, Michelle K ; Altschuld, Ruth A ; Marban, Eduardo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-dab706c0aa74affabd0b727efc54d17ed9a0e35688feda9d52ab25588bd0ce533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adrenergic beta-Agonists - pharmacology</topic><topic>Animals</topic><topic>Calcium - metabolism</topic><topic>Disease Models, Animal</topic><topic>Heart Failure - complications</topic><topic>Heart Failure - physiopathology</topic><topic>Heart Ventricles - drug effects</topic><topic>Heart Ventricles - physiopathology</topic><topic>Hypertension - complications</topic><topic>In Vitro Techniques</topic><topic>Male</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocardium - metabolism</topic><topic>Perfusion</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Stress, Mechanical</topic><topic>Temperature</topic><topic>Ventricular Dysfunction, Left - physiopathology</topic><topic>Ventricular Function, Right - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Janssen, Paul M. L</creatorcontrib><creatorcontrib>Stull, Linda B</creatorcontrib><creatorcontrib>Leppo, Michelle K</creatorcontrib><creatorcontrib>Altschuld, Ruth A</creatorcontrib><creatorcontrib>Marban, Eduardo</creatorcontrib><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>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Janssen, Paul M. L</au><au>Stull, Linda B</au><au>Leppo, Michelle K</au><au>Altschuld, Ruth A</au><au>Marban, Eduardo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Selective contractile dysfunction of left, not right, ventricular myocardium in the SHHF rat</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2003-03-01</date><risdate>2003</risdate><volume>284</volume><issue>3</issue><spage>H772</spage><epage>H778</epage><pages>H772-H778</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><abstract>1 Institute of Molecular Cardiobiology, Johns
Hopkins University School of Medicine, Baltimore, Maryland 21205;
and 2 Department of Physiology and Cell Biology and
3 Dorothy M. Davis Heart and Lung Institute, Ohio
State University, Columbus, Ohio 43210
The progression of hypertension to
cardiac failure involves systemic changes that may ultimately affect
contractility throughout the heart. Spontaneous hypertensive heart
failure (SHHF) rats have depressed left ventricular (LV) function, but
right ventricular (RV) dysfunction is less well characterized.
Ultrathin (87 ± 5 µm) trabeculae were isolated from end-stage
failing SHHF rats and from age-matched controls. Under
near-physiological conditions (1 mM Ca 2+ , 37°C, 4 Hz),
developed force (in mN/mm 2 ) was not significantly different
in SHHF LV and RV trabeculae and those of controls. SHHF LV
preparations displayed a negative force-frequency behavior (40 ± 7 vs. 23 ± 4 mN/mm 2 , 2 vs. 7 Hz); this relationship
was positive in SHHF RV preparations (27 ± 5 vs. 40 ± 6 mN/mm 2 ) and controls (32 ± 6 vs. 44 ± 9 mN/mm 2 ). The response to isoproterenol (10 6
M, 4 Hz) was depressed in SHHF LV preparations. The inotropic response
to hypothermia was lost in SHHF LV trabeculae but preserved in SHHF RV
trabeculae. Intracellular calcium measurements revealed impaired
calcium handling at higher frequencies in LV preparations. We conclude
that in end-stage failing SHHF rats, RV function is only marginally
affected, whereas a severe contractile dysfunction of LV myocardium is present.
contractile function; excitation-contraction coupling; heart
failure; inotropic agents; hypertension</abstract><cop>United States</cop><pmid>12424099</pmid><doi>10.1152/ajpheart.01061.2001</doi></addata></record> |
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| issn | 0363-6135 1522-1539 |
| language | eng |
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| source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Adrenergic beta-Agonists - pharmacology Animals Calcium - metabolism Disease Models, Animal Heart Failure - complications Heart Failure - physiopathology Heart Ventricles - drug effects Heart Ventricles - physiopathology Hypertension - complications In Vitro Techniques Male Myocardial Contraction - drug effects Myocardium - metabolism Perfusion Rats Rats, Inbred Strains Stress, Mechanical Temperature Ventricular Dysfunction, Left - physiopathology Ventricular Function, Right - drug effects |
| title | Selective contractile dysfunction of left, not right, ventricular myocardium in the SHHF rat |
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