Arrhythmogenic properties of the ventricular myocardium in cardiomyopathic Syrian hamster, BIO 14.6 strain

Hano, Osamu; Mitsuoka, Takao; Matsumoto, Yoriaki; Ahmed, Rehan; Hirata, Masanobu; Hirata, Toshifumi; Mori, Mitsuhiro; Yano, Katsusuke; Hashiba, Kunitake

doi:10.1093/cvr/25.1.49

Cited by 22 publications

(10 citation statements)

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“…Therefore, we assumed that the hamsters with cardiomyopathy may have died suddenly due to arrhythmias that are frequently associated with the progression of cardiomyopathy. 21) These results suggest that the third-generation β-blocker carvedilol, which acts as a nonselective β-blocker, an β-blocker, and an antioxidant, could prevent cardiac events and thus prolong survival.…”

Section: Survival Ratementioning

confidence: 82%

<b>Carvedilol Prevents Myocardial Fibrosis in Hamsters</b>

et al. 2006

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SUMMARYThe objective of the present study was to determine if carvedilol protects against myocardial degeneration and fibrotic change, and reduces mortality in TO2 hamsters.Carvedilol was administered intraperitoneally to 8 week-old TO2 hamsters for 21 weeks at a dose of 11 mg/kg/day. There were 15 TO2 hamsters in the carvedilol group (group C) and 10 in the untreated group (group N). The control group consisted of 11 Fb hamsters (group F). The mortality rate was determined from the number of surviving hamsters after 29 weeks. Myocardial fibrosis was evaluated by MRI and histopathological examination. EF and LVDd were determined by echocardiography at 8 and 29 weeks, while the MRI score was calculated at 29 weeks.Mortality, histopathological fibrosis, and MRI score were all lower in group C than in group N. Carvedilol had a protective effect against myocardial fibrosis and decreased the mortality rate in TO2 hamsters. ( 2-4) Following this, β-blocker therapy became used for the treatment of chronic heart failure.We previously performed MRI studies in a hamster model of cardiomyopathy (Bio 14.6 hamster) and found abnormal sites of enhancement as well as delayed enhancement. We proposed that the enhanced areas were regions of myocardial degeneration and fibrosis. 5) Carvedilol is a β-blocker that also has α-blocking and antioxidant effects, which have been shown to reduce the mortality rate of patients with moderate to severe chronic cardiac failure by 35% to 65%, in addition to also lowering the rehospitalization rate. 3,4) In the present study, we assessed the effects of carvedilol [6][7][8] in another hamster model of dilated cardiomyopathy, the BioFrom the

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Section: Survival Ratementioning

confidence: 82%

<b>Carvedilol Prevents Myocardial Fibrosis in Hamsters</b>

et al. 2006

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“…15 Numerous studies have indicated that electrophysiological remodeling such as changes of action potential, K ϩ , and Ca 2ϩ currents occurs in hypertrophy and heart failure (see review by Tomaselli and Marbán 7 ). Thuringer et al 5,6 reported that the I to and I Ca,L densities were decreased and the APD was prolonged in ventricular cells isolated from MS 200 Syrian hamsters in which dilated cardiomyopathy develops without any detectable hypertrophic phase.…”

Section: Matsumoto Et Al Et a Receptor Blockade On Electrical Remodelingmentioning

confidence: 99%

“…12,13 More recently it has been found that long-term treatment with TA-0201, a selective ET A antagonist, 14 improved cardiac function and survival rate in cardiomyopathic Syrian hamsters. 11 Since the BIO 14.6 cardiomyopathic hamsters were reported to have ventricular arrhythmias in the late stage, 15 the ET A receptor antagonist might prevent sudden cardiac death by inhibiting electrophysiological alterations associated with cardiomyopathic contractile dysfunction. Therefore, the present study was undertaken to examine the effect of long-term ET A receptor blockade on the electrophysiological properties of ventricular cells, the surface ECG, and the survival rate in cardiomyopathic Syrian hamsters.…”

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confidence: 99%

Long-Term Endothelin A Receptor Blockade Inhibits Electrical Remodeling in Cardiomyopathic Hamsters

Matsumoto

Aihara²,

Yamauchi-Kohno³

et al. 2002

Circulation

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Background-The endothelin (ET) system is activated in failing hearts. Congestive heart failure frequently is associated with ventricular arrhythmias, which may result from electrical remodeling such as changes of ionic current density and heterogeneous action potential prolongation. We examined the effects of long-term ET A receptor blockade on the electrophysiological properties of ventricular cells, the surface ECG, and the survival in BIO 14.6 cardiomyopathic hamsters. Methods and Results-Membrane currents and action potentials were recorded from left ventricular cells isolated from normal F1␤ hamsters and cardiomyopathic BIO 14.6 hamsters untreated and chronically treated with TA-0201, an ET A receptor antagonist. In ventricular cells of untreated BIO 14.6 hamsters, the action potential duration was prolonged and the densities of the L-type Ca 2ϩ current (I Ca,L ), the transient outward current (I to ), the delayed rectifier K ϩ current (I K ), and the inward rectifier K ϩ current (I K1 ) were decreased compared with those of F1␤ hamsters. Long-term treatment with the ET A receptor antagonist significantly attenuated action potential duration prolongation and reduction of I to , I K , and I Ca,L in BIO 14.6 ventricular cells. Long-term ET A receptor blockade prevented the QT prolongation and ventricular arrhythmias and improved the survival rate in the cardiomyopathic hamsters. Conclusions-Long-term treatment with an ET

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“…Nevertheless, the present data support the view that biochemical and compositional changes occurring in cardiac membranes of cardiomyopathic hamsters could be related with the pathophysiology of the Syrian hamster cardiomyopathy. In fact, an overall defect in membrane composition could lead to the onset of electrolyte imbalance [16,37] in the early stages of cardiomyopathy and, later, to arrhythmias [38] and necrosis of the tissue.…”

Section: Discussionmentioning

confidence: 99%

Phospholipid base exchange enzyme activity in sarcolemmal membranes from the heart of cardiomyopathic hamsters

et al. 1992

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The activity of phospholipid base exchange enzymes has been evaluated in cardiac sarcolemmal membranes from Syrian Golden hamsters and from a hamster strain (UM-X7.1) characterized by a genetic form of hypertrophic cardiomyopathy. No choline base exchange activity and only a little serine base exchange activity were detected, whereas the ethanolamine base exchange enzyme was found highly active in membranes from both strains. For this reason, the present study is focussed on the ethanolamine base exchange enzyme. The apparent Km for ethanolamine of ethanolamine base exchange enzyme from Syrian Golden membranes and from UM-X7.1 strain membranes are 18 and 32 microM, respectively. The specific activity of the sarcolemmal ethanolamine base exchange enzyme is lower in the UM-X7.1 strain than in Syrian Golden hamsters. The calcium-dependence of the enzyme appears different when the membranes from the two strains are compared. Indeed, after removal of the membrane-bound divalent cations, comparable activities are found in both membrane preparations, whereas, upon addition of Ca2+ to the incubation mixtures, the activity of the enzyme is enhanced in the membranes from Syrian Golden strain more than in those from UM-X7.1 strain. The cholesterol content of sarcolemmal membranes is higher in the cardiomyopathic strain than in the Syrian Golden hamsters. A possible relation between changes of the membrane lipid composition and of the ethanolamine base exchange activity is discussed.

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Arrhythmogenic properties of the ventricular myocardium in cardiomyopathic Syrian hamster, BIO 14.6 strain

Abstract: This study provides the first evidence of the high arrhythmogenicity of the ventricles in cardiomyopathic hamsters.

Cited by 22 publications

References 0 publications

<b>Carvedilol Prevents Myocardial Fibrosis in Hamsters</b>

<b>Carvedilol Prevents Myocardial Fibrosis in Hamsters</b>

Long-Term Endothelin A Receptor Blockade Inhibits Electrical Remodeling in Cardiomyopathic Hamsters

Phospholipid base exchange enzyme activity in sarcolemmal membranes from the heart of cardiomyopathic hamsters

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