Rat model of exercise-induced cardiac hypertrophy: hemodynamic characterization using left ventricular pressure-volume analysis. - Wikidata - awgldk - TriplyDB

Rat model of exercise-induced cardiac hypertrophy: hemodynamic characterization using left ventricular pressure-volume analysis.

Rat model of exercise-induced cardiac hypertrophy: hemodynamic characterization using left ventricular pressure-volume analysis.

http://www.wikidata.org/entity/Q44096043

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Effects of hypertension and exercise on cardiac proteome remodelling Increased stiffness is the major early abnormality in a pig model of severe aortic stenosis and predisposes to congestive heart failure in the absence of systolic dysfunction.The soluble guanylate cyclase activator cinaciguat prevents cardiac dysfunction in a rat model of type-1 diabetes mellitus Knockout of p21-activated kinase-1 attenuates exercise-induced cardiac remodelling through altered calcineurin signalling Cardiac fibrosis and down regulation of GLUT4 in experimental diabetic cardiomyopathy are ameliorated by chronic exposures to intermittent altitude Cinaciguat prevents the development of pathologic hypertrophy in a rat model of left ventricular pressure overload.Swimming exercise changes hemodynamic responses evoked by blockade of excitatory amino receptors in the rostral ventrolateral medulla in spontaneously hypertensive rats Prevention of the development of heart failure with preserved ejection fraction by the phosphodiesterase-5A inhibitor vardenafil in rats with type 2 diabetes.Humanized animal exercise model for clinical implication.Association of Exercise Training with Tobacco Smoking Prevents Fibrosis but has Adverse Impact on Myocardial Mechanics.Physiological and pathological left ventricular hypertrophy of comparable degree is associated with characteristic differences of in vivo hemodynamics.Diastolic dysfunction in prediabetic male rats: Role of mitochondrial oxidative stress.Prevention against renal damage in rats with subtotal nephrectomy by sacubitril/valsartan (LCZ696), a dual-acting angiotensin receptor-neprilysin inhibitor.Acute and Chronic Exercise in Animal Models.Comparison of speckle-tracking echocardiography with invasive hemodynamics for the detection of characteristic cardiac dysfunction in type-1 and type-2 diabetic rat models.Strain and strain rate by speckle-tracking echocardiography correlate with pressure-volume loop-derived contractility indices in a rat model of athlete's heart.A comparison of passive hindlimb cycling and active upper-limb exercise provides new insights into systolic dysfunction after spinal cord injury.Temporal analysis of cardiovascular control and function following incomplete T3 and T10 spinal cord injury in rodents.

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Rat model of exercise-induced cardiac hypertrophy: hemodynamic characterization using left ventricular pressure-volume analysis.

http://www.wikidata.org/entity/Q44096043

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2013 nî lūn-bûn

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AJPHEART.00108.2013

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American Journal of Physiology - Heart and Circulatory Physiology

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Rat model of exercise-induced ...... ular pressure-volume analysis.

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Attila Oláh

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Balázs Tamás Németh

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Béla Merkely

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Dalma Kellermayer

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Gábor Szabó

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László Hidi

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Tamás Radovits

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Árpád Lux

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P2860

Measurement of cardiac function using pressure-volume conductance catheter technique in mice and rats

Physiological cardiac remodelling in response to endurance exercise training: cellular and molecular mechanisms

The heart of trained athletes: cardiac remodeling and the risks of sports, including sudden death

Cardiac arrhythmogenic remodeling in a rat model of long-term intensive exercise training

Geometrical models for cardiac MRI in rodents: comparison of quantification of left ventricular volumes and function by various geometrical models with a full-volume MRI data set in rodents.

Athlete's heart.

Cardiac energetics: from E(max) to pressure-volume area.

Chronic CaMKII inhibition blunts the cardiac contractile response to exercise training

Ventriculo-arterial coupling: concepts, assumptions, and applications.

Phosphoinositide 3-kinase(p110alpha) plays a critical role for the induction of physiological, but not pathological, cardiac hypertrophy.

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10.1152/AJPHEART.00108.2013

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