Effects of aging on the cardiac remodeling induced by chronic high-altitude hypoxia in rat

Chouabe, Christophe; Ricci, E.; Amsellem, Jacqueline; Blaineau, S.; Dalmaz, Y.; Favier, R.; Pequignot, J.-M.; Bonvallet, Robert

doi:10.1152/ajpheart.00199.2004

Cited by 17 publications

(17 citation statements)

References 42 publications

(61 reference statements)

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“…A decrease in the transient outward potassium current (Ito) density was observed in RV cell only in the 2-month-old exposed group. The norepinephrine content in the RV was decreased in each age group exposed to hypoxia when compared with their age-matched control group [ 16 ] ( Fig. 9.1 ).…”

Section: The Effects Of Hypoxia On the Heart Experimental Studiesmentioning

confidence: 83%

“…The remodelling (at morphological and electrophysiological levels) induced by chronic hypoxia in the RV can be decreased by the natural aging process [ 16 ]. The extent of RV hypertrophy was less in older animals.…”

Section: The Effects Of Hypoxia On the Heart Experimental Studiesmentioning

confidence: 99%

“…In subjects without severe sign of acute mountain sickness (AMS), high altitude pulmonary edema (HAPE) or high altitude cerebral edema (HACE) [ 16 ]. With permission from the American Physiological Society).…”

Section: Acute Exposure Of Sea Level (Sl) Natives Normal Subjectsmentioning

confidence: 99%

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Right Ventricle and High Altitude

Richalet

Pichon

2014

The Right Heart

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At high altitude, as hypoxia induces pulmonary vasoconstriction and increases ipulmonary arterial pressure, right ventricular (RV) function will be affected. The right ventricular function may be affected directly by the hypoxaemic challenge or indirectly through a pressure overload due, in turn to changes in the pulmonary circulation. Both animal and human studies show that moderate or transient hypoxia results in adaptive changes in right ventricle that are reversible with re-exposure to normoxic conditions and RV dysfunction is mainly due to mechanical overload from the pulmonary circulation. When hypoxia is more severe or more prolonged, it may directly impact ventricular diastolic or systolic function through mechanisms that remain to be unraveled. Chronic exposure to hypoxia in high-altitude natives suffering from Monge's disease may lead to RV hypertrophy, RV failure and overall cardiac failure. The adrenergic system may be involved, as well as HIF, PKC or phospholamban. More studies using the latest imaging technology should give us a better understanding of RV systolic and diastolic function in humans exposed to altitude hypoxia including acute, chronic or chronic intermittent hypoxia.

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Section: The Effects Of Hypoxia On the Heart Experimental Studiesmentioning

confidence: 83%

Section: The Effects Of Hypoxia On the Heart Experimental Studiesmentioning

confidence: 99%

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Right Ventricle and High Altitude

Richalet

Pichon

2014

The Right Heart

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“…Although only a few studies concerning the influence of age on chronic hypoxia-induced structural and functional alterations in the cardiovascular system have been carried out, there is an interesting paper that investigates the effects of aging on the cardiac remodeling induced by chronic highaltitude hypoxia in rats (33). In this study, the extent of right ventricular hypertrophy diminished with age.…”

Section: Senescence and Myocardial Electromechanical Functionmentioning

confidence: 85%

“…In this study, the extent of right ventricular hypertrophy diminished with age. Right ventricular cell size and pericellular fibrosis showed a significant increase in the 2-and 6-mo-old rats exposed to hypoxia compared to control (33). The remodeling at morphological and electrophysiological levels induced by chronic hypoxia in the right ventricle can be decreased by the natural aging process (33).…”

Section: Senescence and Myocardial Electromechanical Functionmentioning

confidence: 90%

Views From Within and Beyond: Narratives of Cardiac Contractile Dysfunction Under Senescence

Yang

Nair

Ren

2005

ENDO

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Senesecence is associated with enhanced risk of cardiovascular diseases. It is generally considered that decline in growth hormones (such as insulin-like growth factor I), intrinsic myocardial and endothelial functions, as well as accumuation of reactive oxygen species with increased age may contribute to cardiovascular senescence. It is believed that heart function, especially cardiac reserve declines with advanced age. However, most experimental and clinical investigations on ventricluar function only included young or adult subjects and failed to address this important age issue in heart pathophysiology. Although senescent but otherwise healthy hearts may possess normal pumping function at the resting or non-stressed state, some aging-associated factors such as accumulation of reactive oxygen species and activation of selective stress signaling pathways may interact with certain risk factors and compromise overall cardiac function. The precise cause and progression of compromised cardiac function in the elderly remain controversial. This review will focus on senescene-related alterations in cardiac contractile function with a special emphasis on oxidative stress and activation of stress signaling.

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Transient outward potassium channel: a heart failure mediator

Feng

Yanggan

2015

Heart Fail Rev

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Transient outward K(+) current (Ito) plays a crucial role in shaping the early phase of repolarization and setting the plateau voltage level of action potential. As a result, it extensively affects membrane current flow in the plateau window. A great body of evidence illustrates a transmural gradient of I to within ventricular wall with much higher density in epicardial than endocardial myocytes, which is important for the physiological ventricular repolarization. In heart failure (HF), this gradient is diminished due to a greater reduction of I to in epicardial myocytes. This attenuates the transmural gradient of early repolarization, facilitating conduction of abnormal impulses originated in the epicardium. In addition, I to reduction prolongs action potential duration and increases intercellular Ca(2+), thus affecting Ca(2+) handling and the excitation-contraction coupling. Furthermore, increased intercellular Ca(2+) could activate CaMKII and calcineurin whose role in cardiac hypertrophy and HF development has been well established. Based on the impact of I to reduction on electrical activity, signal conduction, calcium handling and cardiac function, restoration of I to is likely a potential therapeutic strategy for HF. In this review, we summarize the physiological and pathological role of cardiac I to channel and the potential impact of I to restoration on HF therapy with an emphasis of recent novel findings.

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Effects of aging on the cardiac remodeling induced by chronic high-altitude hypoxia in rat

Cited by 17 publications

References 42 publications

Right Ventricle and High Altitude

Right Ventricle and High Altitude

Views From Within and Beyond: Narratives of Cardiac Contractile Dysfunction Under Senescence

Transient outward potassium channel: a heart failure mediator

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