monocrotaline/atrophy

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Skeletal muscle myosin heavy chain expression in rats with monocrotaline-induced cardiac hypertrophy and failure. Relation to blood flow and degree of muscle atrophy.

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Logáil Isteach / Cláraigh

BACKGROUND In congestive heart failure (CHF) the skeletal muscle of the lower limbs develops a myopathy characterised by atrophy and shift from the slow to the fast type fibres. The mechanisms responsible for these changes are not clear yet. OBJECTIVE We investigated the influence of blood flow and

DHT deteriorates the progression of monocrotaline-induced pulmonary arterial hypertension: effects of endogenous and exogenous androgen.

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Logáil Isteach / Cláraigh

Pulmonary arterial hypertension (PAH) is more popular among females than males. However, female patients exhibit better prognosis than men, sex hormones may partly explain such sex paradox. Estrogens are disease modifiers in PAH, androgen effects on PAH are yet incompletely characterized. In this

Arterial degeneration and glomerular hyalinization in the kidney of monocrotaline-intoxicated rats.

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Logáil Isteach / Cláraigh

Urotensin II receptor antagonist attenuates monocrotaline-induced cardiac hypertrophy in rats.

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Logáil Isteach / Cláraigh

Urotensin II (UII) is a vasoactive peptide with potent cardiovascular effects through a G protein-coupled receptor. Hypoxia stimulates the secretion of UII and atrial natriuretic peptide (ANP). However, the effect of UII on hypoxia-induced cardiac hypertrophy is still controversial. The present

A high-calorie diet attenuates cachexia and adipose tissue inflammation in monocrotaline-induced pulmonary hypertensive rats.

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Logáil Isteach / Cláraigh

BACKGROUND Cardiac cachexia is a catabolic state in which adipose tissue atrophy is accompanied by a proinflammatory state. The molecular mechanisms underlying proinflammatory activation remain, however, largely unknown. In this experimental study, the effect of a high-calorie diet was analyzed in

Alteration of fate of vasoactive autacoids in pulmonary circulation following monocrotaline-induced lung vascular injury in rats.

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Logáil Isteach / Cláraigh

1. To learn how pulmonary vascular injury alters the ability of the lung to metabolize vasoactive autacoids, lung vascular lesions were produced in rats by a single subcutaneous injection of monocrotaline (90 mg kg-1), and the blood pressure responses to angiotensin I (AI), angiotensin II (AII),

Monocrotaline-induced cardiopulmonary damage in rats: amelioration by the angiotensin-converting enzyme inhibitor CL242817.

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Logáil Isteach / Cláraigh

Pulmonary injury induced by the plant alkaloid monocrotaline is partially prevented by the angiotensin-converting enzyme (ACE) inhibitor captopril. CL242817 [(S-[R*,S*])-1-([3-acetylthio]-3-benzoyl-2-methyl-propionyl)- L-proline] is a new orally active ACE inhibitor under evaluation as an

Monocrotaline-induced pulmonary endothelial dysfunction in rats.

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Logáil Isteach / Cláraigh

To study the role of endothelial damage in the pathogenesis of lung injury induced by the pyrrolizidine alkaloid monocrotaline, three functions (angiotensin converting enzyme (ACE) activity, plasminogen activator (PLA) activity, and prostacyclin (PGI2) production) associated with the pulmonary

Heart failure increases atrogin-1 and MuRF1 gene expression in skeletal muscle with fiber type-specific atrophy.

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Logáil Isteach / Cláraigh

Heart failure (HF) is characterized by a reduced tolerance to exercise due to early fatigue and dyspnea; this may be due in part to skeletal muscle myopathy with a shift from slow to fast fibers and loss of muscle mass. Muscle wasting does not occur similarly in all types of muscle fiber, thus we

Downhill exercise training in monocrotaline-injected rats: Effects on echocardiographic and haemodynamic variables and survival.

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Logáil Isteach / Cláraigh

BACKGROUND Eccentric exercise training has been shown to improve muscle force strength without excessive cardiovascular stress. Such an exercise modality deserves to be tested in pulmonary arterial hypertension. OBJECTIVE We aimed to assess the effects of an eccentric training modality on cardiac

[Effect of tetrandrine on pulmonary hypertension induced by monocrotaline in rats].

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Logáil Isteach / Cláraigh

The effects of Tetrandrine (Tet) on intraacinous pulmonary arteries (IAPA) and bemodynamics were studied by means of a rat pulmonary hypertension model induced by monocrotaline. The results showed that Tet could reduce the contractive pressure of pulmonary artery, right ventricle and right atrium of

Myocardiopathy and expression of atrial natriuretic peptide in rats with monocrotaline-induced pulmonary hypertension.

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Logáil Isteach / Cláraigh

Myocardiopathy in rats with monocrotaline (MCT)-induced pulmonary hypertension was investigated morphologically and immunohistochemically. A single subcutaneous injection of MCT (60 mg/kg body weight) to SD rats produced progressive cardiac lesions. Histologically, the lesions were characterized by

Endostatin is protective against monocrotaline-induced right heart disease through the inhibition of T-type Ca(2+) channel.

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Logáil Isteach / Cláraigh

Endostatin (ES), a C-terminal fragment of collagen XVIIIα1, has a potent anti-angiogenic effect. ES prevents tumor proliferation through inhibiting T-type Ca(2+) channel. T-type Ca(2+) channel is re-expressed during heart diseases including monocrotaline (MCT)-induced right heart failure. The

Apoptosis and atrophy in rat slow skeletal muscles in chronic heart failure.

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Logáil Isteach / Cláraigh

Congestive heart failure is characterized by a skeletal muscle myopathy with muscle bulk loss. The mechanisms responsible for these changes are not clear at present. We have investigated the role of apoptosis in the rat "slow" soleus muscle during the development of heart failure, which was induced

Beneficial effects of GH/IGF-1 on skeletal muscle atrophy and function in experimental heart failure.

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Logáil Isteach / Cláraigh

Muscle atrophy is a determinant of exercise capacity in heart failure (CHF). Myocyte apoptosis, triggered by tumor necrosis factor-alpha (TNF-alpha) or its second messenger sphingosine (SPH), is one of the causes of atrophy. Growth hormone (GH) improves hemodynamic and cardiac trophism in several

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