Functional and metabolic properties in hearts from aged spontaneously hypertensive rats.

Mochizuki, Seibu; Yabe, H; Taniguchi, Masayuki; Kudo, Tomoko; Maeno, Hiroshi; Takahashi, Kaoru; Nagano, Makoto

doi:10.1253/jcj.50.1007

Cited by 6 publications

(3 citation statements)

References 18 publications

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“…A common feature of the two models, left ventricular hypertrophy, may increase cardiac susceptibility to a number of stresses including those imposed by diabetes, 467 hypothyroidism, 12 or ischemia. 25 Our results suggest that the hypothyroidism accompanying diabetes has a more profound cardiovascular effect in animals with elevated arterial pressure and that hypertrophied myocardium may be functionally more dependent on thyroid status than is nonhypertrophic heart muscle. This hypothesis is supported by the observation that thyroidectomy reduces left ventricular contractility to a greater extent in the SHR than it does in the Wistar-Kyoto rat.…”

Section: Discussionmentioning

confidence: 63%

Insulin, thyroid hormone, and heart function of diabetic spontaneously hypertensive rat.

Davidoff

Rodgers

1990

Hypertension

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Diabetes impairs cardiac performance more extensively in hypertensive rats than it does in nonhypertensive strains. A "low thyroid state" may contribute to the adverse cardiovascular effects of diabetes in spontaneously hypertensive rats (SHR). We tested this hypothesis by comparing the effects of thyroid hormone with those of insulin treatment on cardiac performance of diabetic SHR. Diabetes was induced with streptozotocin (45 mg/kg). Subsets of diabetic rats were treated with either insulin (10-20 units/kg/day) or triiodothyronine (8-10 /ig/kg/day). Heart rate and systolic arterial pressure were obtained at weekly intervals. After 8 weeks, cardiac function was assessed using an isolated working heart preparation. Diabetes reduced arterial pressure and heart rate in vivo and markedly depressed cardiac performance under volume and pressure loading conditions ex vivo, confirming previous observations. As 4 Chemically induced diabetes in hypertensive rats has a more profound effect on cardiac function than it does in normotensive models. -7Collectively, the data suggest that pressure loadinduced left ventricular hypertrophy increases the susceptibility of the myocardium to diabetes-related derangements.

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Section: Discussionmentioning

confidence: 63%

Insulin, thyroid hormone, and heart function of diabetic spontaneously hypertensive rat.

Davidoff

Rodgers

1990

Hypertension

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“…14,19 On the other hand, only very few data exist concerning the myocardial energy metabolism of aged SHR (Ͼ40 weeks) suffering from progressive myocardial dysfunction. Carlier et al 11 found reduced PCr in the isolated hearts of 72-week-old SHR, and Mochizuki et al 10 in the hearts of 44-week-old SHR after an ischemic period compared with control hearts.…”

Section: Age-dependent Alterations Of Myocardial Performance and Enermentioning

confidence: 97%

Age-related decline of PCr/ATP-ratio in progressively hypertrophied hearts of spontaneously hypertensive rats

et al. 2000

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Although the ultimate cause for the myocardial dysfunction of hypertensive heart disease is still unclear, a crucial role of the myocardial energy metabolism has been suggested. Therefore, the aim of the present study was to investigate whether age-related myocardial dysfunction in hearts of spontaneously hypertensive rats (SHR) is associated with an impaired myocardial energy metabolism. Isolated hearts of SHR and Wistar Kyoto rats (WKY) aged about 40, 60, and 80 weeks, respectively (each n = 4-5), were perfused according to the working heart technique. Cardiac work and coronary flow were monitored online. Myocardial energy metabolism was evaluated by calculating the ratio of phosphocreatine (PCr) and adenosine triphosphate (ATP) which were measured by nuclear magnetic resonance (31P-NMR) spectroscopy. All hearts were subjected to work for 30min at baseline conditions (low afterload), followed by another 30min under a moderate pressure load (high afterload). Each SHR group showed a higher heart weight/body weight ratio than the age-matched WKY controls. The SHR showed a progressive age-dependent reduction of cardiac work (40 weeks = 5.1+/-0.3, 60 weeks = 4.0+/-0.3, 80 weeks = 3.8+/-0.2 (mW/g) at baseline conditions) and PCr/ATP-ratio (40 weeks = 1.82+/-0.06, 60 weeks = 1.69+/-0.05, 80 weeks = 1.59+/-0.09 (PCr/ATP) at baseline conditions). Similar results were found for hearts of SHR at high afterload. In WKY no significant decline in cardiac work or PCr/ATP-ratio was found under either low or under high afterload. The cardiac work capacity of hearts of SHR progressively decreases with increasing age and left ventricular hypertrophy. This myocardial dysfunction is closely associated with an impaired PCr/ATP-ratio, suggesting a decreased energy reserve.

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“…Engelmann et al [79] reported a decrease in the LV capillary density in the SHR at 6 months. A number of investigators have reported decreases in CrP levels in the aging SHR heart [80][81][82]. Bittl and Ingwall [83] reported a 50 % decrease in Cr kinase activity in the 18 month SHR relative to age-matched WKY.…”

Section: Energeticsmentioning

confidence: 99%

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Boluyt

et al. 2002

Heart Failure Reviews

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The spontaneously hypertensive rat (SHR) is an animal model of genetic hypertension which develops heart failure with aging, similar to man. The consistent pattern of a long period of stable hypertrophy followed by a transition to failure provides a useful model to study mechanisms of heart failure with aging and test treatments at differing phases of the disease process. The transition from compensated hypertrophy to failure is accompanied by changes in cardiac function which are associated with altered active and passive mechanical properties of myocardial tissue; these events define the physiologic basis for cardiac decompensation. In examining the mechanism for myocardial tissue dysfunction, studies have demonstrated a central role for neurohormonal activation, and specifically the renin-angiotensin-aldosterone system. Pharmacologic attenuation of this system at differing points in the course of the process suggests that prevention but not reversal of myocardial tissue dysfunction is possible. The roles of the extracellular matrix, apoptosis, intracellular calcium, beta-adrenergic stimulation, microtubules, and oxygen supply-demand relationships in ultimately mediating myocardial tissue dysfunction are reviewed. Studies suggest that while considerable progress has been made in understanding and treating the transition to failure, our current state of knowledge is limited in scope and we are not yet able to define specific mechanisms responsible for tissue dysfunction. It will be necessary to integrate information on the roles of newly discovered, and as yet undiscovered, genes and pathways to provide a clearer understanding of maladaptive remodeling seen with heart failure. Understanding the mechanism for tissue dysfunction is likely to result in more effective treatments for the prevention and reversal of heart failure with aging. It is anticipated that the SHR model will assist us in reaching these important goals.

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Functional and metabolic properties in hearts from aged spontaneously hypertensive rats.

Cited by 6 publications

References 18 publications

Insulin, thyroid hormone, and heart function of diabetic spontaneously hypertensive rat.

Insulin, thyroid hormone, and heart function of diabetic spontaneously hypertensive rat.

Age-related decline of PCr/ATP-ratio in progressively hypertrophied hearts of spontaneously hypertensive rats

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