scholarly journals Ventricular remodeling and function: Insights using murine echocardiography

2010 ◽  
Vol 48 (3) ◽  
pp. 512-517 ◽  
Author(s):  
Marielle Scherrer-Crosbie ◽  
Baptiste Kurtz
Keyword(s):  
Ventricular Remodeling ◽  
And Function ◽  
Murine Echocardiography

Contribution of ventricular remodeling to pathogenesis of heart failure in rats

2001 ◽  
Vol 280 (2) ◽  
pp. H674-H683 ◽  
Author(s):  
Gregory L. Brower ◽  
Joseph S. Janicki
Keyword(s):  
Heart Failure ◽  
Ventricular Remodeling ◽  
Volume Fraction ◽  
Volume Overload ◽  
Left Ventricular ◽  
Morbidity And Mortality ◽  
Compliance Matrix ◽  
Hypertrophic Response ◽  
Lv Volume ◽  
And Function

We previously reported an approximately 50% incidence of rats with symptoms of congestive heart failure (CHF) at 8 wk postinfrarenal aorto-caval fistula. However, it was not clear whether compensatory ventricular remodeling could continue beyond 8 wk or whether the remaining animals would have developed CHF or died. Therefore, the intent of this study was to complete the characterization of this model of sustained volume overload by determining the morbidity and mortality and the temporal response of left ventricular (LV) remodeling and function beyond 8 wk. The findings demonstrate an upper limit to LV hypertrophy and substantial increases in LV volume and compliance, matrix metalloproteinase activity, and collagen volume fraction associated with the development of CHF. There was an 80% incidence of morbidity and mortality following 21 wk of chronic volume overload. These findings indicate that the development of CHF is triggered by marked ventricular dilatation and increased compliance occurring once the myocardial hypertrophic response is exhausted.

Race Differences in Ventricular Remodeling and Function Among College Football Players

2013 ◽  
Vol 112 (1) ◽  
pp. 128-134 ◽  
Author(s):  
Francois Haddad ◽  
Shanon Peter ◽  
Olivia Hulme ◽  
David Liang ◽  
Ingela Schnittger ◽  
...  
Keyword(s):  
Ventricular Remodeling ◽  
College Football ◽  
Race Differences ◽  
Football Players ◽  
And Function

Adenylyl cyclase activity and function are decreased in rat cardiac fibroblasts after myocardial infarction

2007 ◽  
Vol 293 (5) ◽  
pp. H3216-H3220 ◽  
Author(s):  
James S. Swaney ◽  
Hemal H. Patel ◽  
Utako Yokoyama ◽  
N. Chin Lai ◽  
Matthew Spellman ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Adenylyl Cyclase ◽  
Collagen Synthesis ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Cardiac Fibroblasts ◽  
Left Ventricular ◽  
Collagen Production ◽  
And Function ◽  
Expression And Activity

Myocardial infarction (MI) results in left ventricular remodeling (e.g., ventricular hypertrophy, dilatation, and fibrosis). Fibrosis contributes to increased myocardial stiffening, impaired ventricular filling and function, and reduced cardiac output. Adenylyl cyclase (AC) expression and activity are reduced in animal models of heart failure. Stimulation of AC can inhibit extracellular matrix production in isolated cardiac fibroblasts; however, a role for reduced AC expression and activity in fibrosis associated with cardiac remodeling after chronic MI has never been determined. We tested the hypothesis that AC expression and activity are reduced in cardiac fibroblasts after chronic (18 wk) MI. Rats underwent coronary artery ligation or sham surgery (control), and echocardiography was used to assess left ventricular remodeling 1, 3, 5, 7, 10, 12, and 18 wk after surgery. Cardiac fibroblasts were isolated from the noninfarcted myocardium and compared for differences in AC activity and collagen synthesis. End-diastolic dimension was increased [control: 0.76 ± 0.02 cm and MI: 1.0 ± 0.02 cm (means ± SE), P < 0.001] and fractional shortening was decreased (control: 44 ± 2% and MI: 17 ± 2%, P < 0.001) in MI compared with control rats. Basal and forskolin-stimulated cAMP production were decreased by 90% and 93%, respectively, and AC5/6 expression was decreased 39% in fibroblasts isolated from MI rats compared with sham controls. Serum-stimulated collagen production was increased twofold and forskolin-mediated inhibition of collagen synthesis was reduced in fibroblasts from MI rats compared with controls. Our data demonstrate that AC expression and activity are reduced and collagen production is increased in cardiac fibroblasts of rats after MI.

scholarly journals Impaired contractile function and calcium handling in hearts of cardiac-specific calcineurin b1-deficient mice

2009 ◽  
Vol 297 (4) ◽  
pp. H1263-H1273 ◽  
Author(s):  
Paul J. Schaeffer ◽  
Jaime DeSantiago ◽  
John Yang ◽  
Thomas P. Flagg ◽  
Attila Kovacs ◽  
...  
Keyword(s):  
Ventricular Remodeling ◽  
Contractile Function ◽  
Postnatal Growth ◽  
Calcium Handling ◽  
Regulatory Subunit ◽  
Plasmic Reticulum ◽  
Diastolic Relaxation ◽  
And Function ◽  
Cardiac Maturation ◽  
Functional Phenotype

To define the necessity of calcineurin (Cn) signaling for cardiac maturation and function, the postnatal phenotype of mice with cardiac-specific targeted ablation of the Cn B1 regulatory subunit (Ppp3r1) gene (csCnb1−/− mice) was characterized. csCnb1−/− mice develop a lethal cardiomyopathy, characterized by impaired postnatal growth of the heart and combined systolic and diastolic relaxation abnormalities, despite a lack of structural derangements. Notably, the csCnb1−/− hearts did not exhibit diastolic dilatation, despite the severe functional phenotype. Myocytes isolated from the mutant mice exhibited reduced rates of contraction/relaxation and abnormalities in calcium transients, consistent with altered sarcoplasmic reticulum loading. Levels of sarco(endo) plasmic reticulum Ca-ATPase 2a (Atp2a2) and phospholamban were normal, but phospholamban phosphorylation was markedly reduced at Ser16 and Thr17. In addition, levels of the Na/Ca exchanger (Slc8a1) were modestly reduced. These results define a novel mouse model of cardiac-specific Cn deficiency and demonstrate novel links between Cn signaling, postnatal growth of the heart, pathological ventricular remodeling, and excitation-contraction coupling.

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