Nebivolol enhances survival of cardiomyopathic hamsters with congestive heart failure

1992 ◽  
Vol 24 ◽  
pp. S56
Author(s):  
L VERDONCK
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiomyopathic Hamsters

Nebivolol Increases Survival in Cardiomyopathic Hamsters with Congestive Heart Failure

1991 ◽  
Vol 18 (1) ◽  
pp. 1-3 ◽  
Author(s):  
Luc Ver Donck ◽  
Luc Wouters ◽  
Hans G. Olbrich ◽  
Ernst Mutschler ◽  
Marcel Borgers
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiomyopathic Hamsters

Effect of Nebivolol on Survival of Cardiomyopathic Hamsters with Congestive Heart Failure

1991 ◽  
Vol 3 (S1) ◽  
pp. 82-85
Author(s):  
Luc Donck ◽  
L. Wouters ◽  
H. G. Olbrich ◽  
E. Mutschler ◽  
M. Borgers ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiomyopathic Hamsters

Systemic and Regional Hemodynamic and Cardiac Remodeling Effects of Candesartan in Dilated Cardiomyopathic Hamsters With Advanced Congestive Heart Failure

2002 ◽  
Vol 40 (2) ◽  
pp. 189-200 ◽  
Author(s):  
Sonia Goineau ◽  
Sophie Nisse-Durgeat ◽  
Danielle Pape ◽  
Pascal Guillo ◽  
Marie-Paule Ramée ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiac Remodeling ◽  
Cardiomyopathic Hamsters

Atrial natriuretic factor binding sites in experimental congestive heart failure

1989 ◽  
Vol 257 (4) ◽  
pp. F515-F523
Author(s):  
C. Bianchi ◽  
G. Thibault ◽  
E. Wrobel-Konrad ◽  
A. De Lean ◽  
J. Genest ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Binding Sites ◽  
Atrial Natriuretic Factor ◽  
Severe Heart Failure ◽  
Zona Glomerulosa ◽  
Renal Glomeruli ◽  
Natriuretic Factor ◽  
Cardiomyopathic Hamsters ◽  
Atrial Natriuretic

A quantitative in vitro autoradiographic study was performed on the aorta, renal glomeruli, and adrenal cortex of cardiomyopathic hamsters in various stages of heart failure and correlated, in some instances, with in vivo autoradiography. The results indicate virtually no correlation between the degree of congestive heart failure and the density of 125I-labeled atrial natriuretic factor [(Ser99, Tyr126)ANF] binding sites (Bmax) in the tissues examined. Whereas the Bmax was increased in the thoracic aorta in moderate and severe heart failure, there were no significant changes in the zona glomerulosa. The renal glomeruli Bmax was lower in mild and moderate heart failure compared with control and severe heart failure. The proportion of ANF B- and C-receptors was also evaluated in sections of the aorta, adrenal, and kidney of control and cardiomyopathic hamsters with severe heart failure. (Arg102, Cys121)ANF [des-(Gln113, Ser114, Gly115, Leu116, Gly117) NH2] (C-ANF) at 10(-6) M displaced approximately 505 of (Ser99, Tyr126)125I-ANF bound in the aorta and renal glomeruli and approximately 20% in the adrenal zona glomerulosa in both series of animals. These results suggest that ANF may exert a buffering effect on the vasoconstriction of heart failure and to a certain extent may inhibit aldosterone secretion. The impairment of renal sodium excretion does not appear to be related to glomerular ANF binding sites at any stage of the disease.

Matrix remodeling in experimental and human heart failure: a possible regulatory role for TIMP-3

2003 ◽  
Vol 284 (2) ◽  
pp. H626-H634 ◽  
Author(s):  
Paul W. M. Fedak ◽  
Svetlana M. Altamentova ◽  
Richard D. Weisel ◽  
Nafiseh Nili ◽  
Nobuhisa Ohno ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Human Heart ◽  
Matrix Remodeling ◽  
Human Heart Failure ◽  
Protein Levels ◽  
Cardiomyopathic Hamsters ◽  
End Stage ◽  
Myocardial Collagen ◽  
Normal Controls

In the failing heart, an imbalance in matrix metalloproteinases (MMPs) and their biological regulators, the tissue inhibitors of MMPs (TIMPs), may result in cardiac dilatation from matrix degradation. We hypothesized that a reduction of myocardial TIMP-3 is associated with adverse matrix remodeling in both human and experimental heart failure. Cardiomyopathic hamsters at age 15 wk (normal), 25 wk (compensated stage), and 35 wk (overt failure) were compared with age-matched normal controls. MMP activity (gelatinase bioassay) was increased in cardiomyopathic hearts ( P = 0.03) and peaked during the transition to overt heart failure. TIMP-3 content (immunoblot) was decreased compared with normal controls (74 ± 5% at 25 wk, 69 ± 10% at 35 wk; P = 0.001) and its reduction was associated with increased MMP activity ( r = −0.6; P = 0.004). TIMP-1 increased progressively ( P = 0.001), whereas TIMP-2, TIMP-4, and MMP protein levels were unchanged. Myocardial collagen (hydroxyproline content) increased with time during the progression to end-stage cardiac failure ( P < 0.0001). Collagen synthesis ([14C]proline uptake) was elevated in cardiomyopathy at 15 and 25 wk ( P < 0.05). The collagen cross-linking ratio (insoluble:soluble collagen) was reduced ( P = 0.003) as the left ventricle dilated. By confocal microscopy restricted to viable myocardium, collagen content was reduced ( P = 0.04) with fragmentation ( P < 0.0001) and thinning ( P = 0.003) of perimysial collagen fibers. Similarly, patients with end-stage congestive heart failure ( n = 7) compared with nonfailing controls ( n = 2) had elevated gelatinase MMP activity ( P = 0.02) associated with isolated reductions in TIMP-3 (55 ± 5% of normal; P = 0.003). Reductions of TIMP-3 parallel adverse matrix remodeling in the cardiomyopathic hamster and the failing human heart. TIMP-3 may contribute to the regulation of myocardial remodeling and its reduction may promote a transition from compensated to end-stage congestive heart failure.

Nonselective ETA/ETB-receptor blockade increases systemic blood pressure of Bio 14.6 cardiomyopathic hamstersThis article is one of a selection of papers published in the special issue (part 1 of 2) on Forefronts in Endothelin.

2008 ◽  
Vol 86 (6) ◽  
pp. 394-401 ◽  
Author(s):  
Jean-Claude Honoré ◽  
Émilie Carrier ◽  
Marie-Hélène Fecteau ◽  
Carlos R. Tirapelli ◽  
Ghassan Bkaily ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Congestive Heart Failure ◽  
Systemic Blood Pressure ◽  
Left Ventricular ◽  
Receptor Blockade ◽  
Receptor Antagonists ◽  
Systemic Blood ◽  
Receptor Antagonism ◽  
Cardiomyopathic Hamsters

To examine the role of endothelin ETA and ETB receptors in congestive heart failure due to cardiomyopathy, the effect of chronic treatment with selective ETA- and ETB-receptor antagonists (atrasentan and A-192621, respectively), alone and in combination, was assessed on functional and biochemical parameters of 52-week-old Bio 14.6 cardiomyopathic hamsters. Compared with control animals, cardiomyopathic hamsters treated for 9 weeks with atrasentan showed no variation in MAP; however, selective ETB- and combined nonselective ETA- and ETB-receptor antagonists increased systemic blood pressure. After selective ETB-receptor blockade, plasma endothelin levels were augmented. Importantly, this increase was highly enhanced (more than 8-fold) by concomitant ETA-receptor antagonism. Furthermore, the left ventricle : body weight ratio of cardiomyopathic hamsters treated with A-192621, alone or in combination with atrasentan, was significantly increased. On the other hand, decreased left ventricular end-diastolic pressure was observed in cardiomyopathic hamsters after selective ETA- or combined nonselective ETA/ETB-receptor antagonism, while only selective ETA-receptor blockade reduced left ventricular endothelin levels. Our results suggest that, in congestive heart failure, ETB receptors are essential to limit circulating endothelin levels, which may argue for improved cardiac benefits after long-term treatment with highly selective ETA-receptor antagonists.

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