Myocardial Fibrosis and Stiffness With Hypertrophy and Heart Failure in the Spontaneously Hypertensive Rat

Conrad, Chester H.; Brooks, Wesley W.; Hayes, J. A.; Sen, Subha; Robinson, Kathleen G.; Bing, O.

doi:10.1161/01.cir.91.1.161

Cited by 385 publications

(286 citation statements)

References 43 publications

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“…Our results are also consistent with investigations showing that cardioprotective treatments are mediated by a restoration or up-regulation of antioxidant enzymes (42,45). It is recognized that an increase in collagen concentration is an integral part of the extracellular matrix remodeling that takes place in the LVs during the natural aging process (66) and as well as in response to a variety of pathologies resulting in hypertrophy of this chamber (67,68). In accordance with these studies, we showed evidence of an increase of collagen deposition with aging and its exacerbation in aged SHR.…”

Section: Discussionsupporting

confidence: 92%

Is Cardiac Hypertrophy in Spontaneously Hypertensive Rats the Cause or the Consequence of Oxidative Stress?

et al. 2008

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The aim of this work was to assess the possible correlation between oxidative damage and the development of cardiac hypertrophy in heart tissue from young (40-d-old) and older (4-, 11-and 19-month-old) spontaneously hypertensive rats (SHR) in comparison with age-matched Wistar (W) rats. To this end, levels of thiobarbituric acid reactive substances (TBARS), nitrotyrosine contents, NAD(P)H oxidase activity, superoxide production, and the activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were determined. Compared to age-matched normotensive rats, SHR showed a significant increase in systolic blood pressure from 40 d of age and left ventricular hypertrophy (LVH) was significantly evident from 4 months of age. W rats (11-and 19-month-old) also showed an increase in LVH with aging. TBARS and nitrotyrosine levels were similar in young rats from both strains and were significantly increased with age in both strains, with the values in SHR being significantly higher than those in age-matched W rats. NAD(P)H activity was similar in young SHR and W rats, whereas it was higher in aged SHR compared with age-matched W rats. Compared to W rats, superoxide production was higher in aged SHR, and was abolished by NAD(P)H inhibition with apocynin. CAT activity was increased in the hearts of 4-month-old SHR compared to age-matched W rats and was decreased in the hearts of the oldest SHR compared to the oldest W rats. SOD and GPx activities decreased in both rat strains with aging. Moreover, an increase in collagen deposition with aging was evident in both rat strains. Taken together, these data showed that aged SHR exhibited higher cardiac hypertrophy and oxidative damage compared to W rats, indicating that the two undesirable effects are associated. That is, oxidative stress appears to be a cause and/or consequence of hypertrophy development in this animal model. (Hypertens Res 2008; 31: 1465-1476)

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Section: Discussionsupporting

confidence: 92%

Is Cardiac Hypertrophy in Spontaneously Hypertensive Rats the Cause or the Consequence of Oxidative Stress?

et al. 2008

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“…However, in the non-compensatory phase, fibrosis and stiffness of the myocardial interstitium were suppressed by BPS administration and diastolic function was maintained [3,24]. The changing point from the compensatory phase to the non-compensatory phase was determined by arterial stiffness induced by pressure overload or cardiac hypertrophy through coronary circulation failure [4,10]. BPS effectively suppresses myocardial degeneration and fibrosis in chronic heart failure by improvement of coronary circulation and an anticytokine effect.…”

Section: Discussionmentioning

confidence: 99%

Effect of Long-term Administration of a Prostacyclin Analogue (Beraprost Sodium) on Myocardial Fibrosis in Dahl Rats

Kaneshige

Saida

Tanaka

et al. 2007

The Journal of Veterinary Medical Science

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ABSTRACT. Beraprost sodium (BPS) is an orally active prostacyclin analogue. The effects of BPS on the heart, including coronary circulation improvement, myocardial and vascular protection and anti-fibrosis effect on myocardium interstitium, have previously been demonstrated. However, the effects of BPS on hemodynamics, cardiac function and myocardial contractility in patients in the hypertrophic phase have not been clarified. Therefore, in the present study, the effects of BPS under long-term administration were investigated using the hypertension model of salt-sensitive Dahl rats. Six-week-old Dahl rats were divided into three groups, an 8% high salt diet group treated with BPS (BPS group), an untreated 8% high salt diet group (HHF group) and an untreated 0.3% low salt diet group (Control group), and observations were conducted until 17 weeks of age. In the BPS and HHF groups, the survival rates after 11 weeks of high salt diet intake were 87.5% and 47.1%, respectively (p<0.05). At 17 weeks of age, the atrial systolic peak velocity/early diastolic peak velocity and heart weight index of the BPS group decreased significantly compared with the HHF group (p<0.05). The HHF group exhibited significantly more severe myocardial fibrosis mainly in the endocardial layer of the left and right ventricles compared with the BPS and Control groups (p<0.05). In the present study, long-term BPS administration preserved diastolic function and prevented myocardial interstitial fibrosis in the non-compensatory phase. The results of the present study suggest that BPS is effective for treatment of hypertensive cardiac hypertrophy. KEY WORDS: beraprost sodium, Dahl rat, echocardiography, hypertension, myocardial fibrosis.J. Vet. Med. Sci. 69(12): 1271-1276, 2007 Prostacyclin is found in all body tissues and body fluids and is the major metabolite of arachidonic acid in the vasculature [6,16]. It is a potent vasodilator that affects both systemic and pulmonary circulations. Prostacyclin also prevents vascular smooth muscle proliferation and inhibits platelet adhesion and aggregation [6]. These features make it a very attractive substance for treatment of various cardiovascular diseases [6,15,16,20]. Beraprost sodium (BPS) is an orally active prostacyclin analogue that was discovered and developed by Toray Industries in Japan [1,16]. In human medicine, long-term administration of BPS has been approved as a treatment for chronic arterial occlusion [16] and primary pulmonary hypertension [2,8,16]. In addition, oral administration of BPS can be used as a therapeutic treatment for secondary precapillary pulmonary hypertension [17], cerebral infarction [9,13], glomerulonephritis [12,28], diabetic nephropathy [29] and atherosclerotic vascular damage in coronary artery disease [23]. In heart failure with pressure overload, compensated concentric hypertrophy in the left ventricular progresses due to the increase in pressure after overload. As a result, then the interstitial fibrosis changes the myocardial structure [21,26,27]. In addition, th...

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“…The first studies for the clinical detection of heart failure signs in rats were carried out by Bing and cols. that studied spontaneously hypertensive rats with heart dysfunction [68][69][70] . The data on the incidence of post-infarction heart failure and the possibility of its clinical recognition in rats, however, are scarce.…”

Section: Morphological Functional and Clinical Evaluation Of Heart Fmentioning

confidence: 99%

Infarto do miocárdio experimental em ratos: análise do modelo

Zornoff¹,

Paiva²,

Minicucci³

et al. 2009

Arq. Bras. Cardiol.

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Myocardial Fibrosis and Stiffness With Hypertrophy and Heart Failure in the Spontaneously Hypertensive Rat

Cited by 385 publications

References 43 publications

Is Cardiac Hypertrophy in Spontaneously Hypertensive Rats the Cause or the Consequence of Oxidative Stress?

Is Cardiac Hypertrophy in Spontaneously Hypertensive Rats the Cause or the Consequence of Oxidative Stress?

Effect of Long-term Administration of a Prostacyclin Analogue (Beraprost Sodium) on Myocardial Fibrosis in Dahl Rats

Infarto do miocárdio experimental em ratos: análise do modelo

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