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hypertrophy/hypoxia
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Dynamic changes of gene expression in hypoxia-induced right ventricular hypertrophy.
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Hypobaric hypoxia induces right ventricular hypertrophy. The relative contribution of pulmonary hypertension, decreased arterial oxygen, and neuroendocrine stimulation to the transcriptional profile of hypoxia-induced right ventricular hypertrophy is unknown. Whereas both ventricles are exposed to
Nocturnal Intermittent Hypoxia Is Associated With Left Ventricular Hypertrophy in Middle-Aged Men With Hypertension and Obstructive Sleep Apnea.
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BACKGROUND
Obstructive sleep apnea (OSA) and left ventricular (LV) hypertrophy are considered to be closely associated. However, the relationship has not yet been fully demonstrated and is hence still controversial. The purpose of this study was to assess in hypertensive male patients the
Nuclear magnetic resonance spectroscopy of rat ventricles following chronic hypoxia: a model of right ventricular hypertrophy.
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Nuclear magnetic resonance spectroscopy was used to study the effect of chronic hypoxia on both right (RV) and left ventricular and septal (LV + S) muscle. Rats in the hypoxic group, kept in a hypobaric chamber at 1/2 atm pressure for 2 weeks, developed right, but not left, ventricular hypertrophy
Regression of left ventricular hypertrophy by converting enzyme inhibition in 12-15-month-old spontaneously hypertensive rats: effects on coronary resistance and ventricular compliance in normoxia and anoxia.
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The effects of trandolapril, a converting enzyme inhibitor (CEI), on left ventricular (LV) diastolic stiffness and coronary vascular resistance (CVR), were studied with an isolated heart preparation in 15-month-old spontaneously hypertensive rats (SHR). The hypertensive animals were treated for 3
Hypoxia-induced cardiac hypertrophy in rabbits treated with verapamil and nifedipine.
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Young rabbits were exposed, eight at a time, to 310 h of hypoxia (O2 at 70-80 torr), at atmospheric pressure. The animals were injected with 1 mg kg-1 nifedipine (F) or 5 mg kg-1 verapamil (V) or an equivalent volume of the vehicle (H) (Cremophor EL), i.p. twice a day. A fourth group (N), also
Effect of verapamil on pulmonary hypertension and right ventricular hypertrophy induced in rats by intermittent high altitude hypoxia.
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Adult male Wistar rats were used for studying the effect of Ca2+ antagonist verapamil on pulmonary hypertension, right ventricular hypertrophy and the medial thickness of pulmonary arterioles, induced by intermittent high altitude (IHA) hypoxia. This was simulated in a hypobaric chamber (7,000, 8 h
The absence of effect of chemical sympathectomy on ventricular hypertrophy induced by hypoxia in young rabbits.
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Young rabbits, eight at a time, were exposed to 203 and 208 h (groups I and II) and 283 and 298 h (groups III and IV) of hypoxia (O2 at 70 to 80 mmHg), at atmospheric pressure. The animals were injected ip with 25 mg X kg-1 on the first day, and with 50 mg X kg-1 on the second day and every 48 h
BAY 41-2272, a direct activator of soluble guanylate cyclase, reduces right ventricular hypertrophy and prevents pulmonary vascular remodeling during chronic hypoxia in neonatal rats.
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Exposure to hypoxia during the first weeks of life in newborn rats decreases vascular growth and alveolarization and causes pulmonary hypertension (PH). BAY 41-2272 is a novel direct activator of soluble guanylate cyclase independent of nitric oxide, effective as an acute pulmonary vasodilator in an
[Various characteristics of the contractile function of the heart in cardiac hypertrophy during readaptation after adaptation of the body to high-altitude hypoxia].
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Hemodynamics, coronary circulation, electric activity and morphologic changes of the heart were investigated in 150 rabbits after their extended adaptation to high altitude hypoxia and during readaptation. It was found that changes in the contractile function of the hypertrophied heart, which
Sustained pulmonary hypertension and right ventricular hypertrophy after chronic hypoxia in mice with congenital deficiency of nitric oxide synthase 3.
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Chronic hypoxia induces pulmonary hypertension and right ventricular (RV) hypertrophy. Nitric oxide (NO) has been proposed to modulate the pulmonary vascular response to hypoxia. We investigated the effects of congenital deficiency of endothelial NO synthase (NOS3) on the pulmonary vascular
Wnt5a attenuates hypoxia-induced pulmonary arteriolar remodeling and right ventricular hypertrophy in mice.
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Hypoxic pulmonary hypertension (HPH), which is characterized by pulmonary arteriolar remodeling and right ventricular hypertrophy, is still a life-threatening disease with the current treatment strategies. The underlying molecular mechanisms of HPH remain unclear. Our previously published study
Sildenafil reverses the hypertrophy of mice right ventricle caused by hypoxia but does not reverse the changes in the myosin heavy chain isoforms
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In this study, we investigated the effect of hypoxia and concomitant sildenafil treatment on MHC isoforms in hypoxia-induced hypertrophied right ventricles. Right ventricular hypertrophy was induced in mice by exposing them to hypoxic stimulus (11% ambient oxygen) in a normobaric chamber for 20
Regression of ventricular hypertrophy abolishes cardiocyte vulnerability to acute hypoxia.
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Left ventricular hypertrophy (LVH) secondary to a pressure overload commonly leads to perfusion abnormalities that may limit oxygen delivery to the myocardium and, therefore, result in cardiocyte intracellular damage. We initiated this study to test the hypothesis that the increased vulnerability of
The influence of pressure overload left ventricular hypertrophy on diastolic properties during hypoxia in isovolumically contracting rat hearts.
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We tested the hypothesis that there is an enhanced susceptibility in hypertrophied cardiac muscle to develop decreased diastolic distensibility of the left ventricle in response to hypoxia. The effects of brief hypoxia (3 minutes) were studied in rats with and without chronic left ventricular
Mild hypoxia induces hypertrophy of cultured neonatal rat cardiomyocytes: a possible endogenous endothelin-1-mediated mechanism.
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Hypoxic or ischemic stresses on cardiomyocytes may cause a variety of compensatory responses including cell hypertrophy. In this study, we examined whether hypoxia induces hypertrophy of cardiomyocytes in vitro and whether hypoxia-induced hypertrophy is inhibited by an endothelin A receptor
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