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monocrotaline/astenia
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Diaphragm weakness in pulmonary arterial hypertension: role of sarcomeric dysfunction.
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We previously demonstrated that diaphragm muscle weakness is present in experimental pulmonary arterial hypertension (PH). However, the nature of this diaphragm weakness is still unknown. Therefore, the aim of this study was to investigate whether changes at the sarcomeric level contribute to
Diaphragm muscle fiber weakness in pulmonary hypertension.
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BACKGROUND
Recently it was suggested that patients with pulmonary hypertension (PH) suffer from inspiratory muscle dysfunction. However, the nature of inspiratory muscle weakness in PH remains unclear.
OBJECTIVE
To assess whether alterations in contractile performance and in morphology of the
Superoxide dismutase/catalase mimetic EUK-134 prevents diaphragm muscle weakness in monocrotalin-induced pulmonary hypertension.
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Patients with pulmonary hypertension (PH) suffer from inspiratory insufficiency, which has been associated with intrinsic contractile dysfunction in diaphragm muscle. Here, we examined the role of redox stress in PH-induced diaphragm weakness by using the novel antioxidant, EUK-134. Male Wistar rats
Pulmonary hypertension in a group of dairy calves.
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An episode of pulmonary arteritis and sclerosis in twenty 5- to 6-month-old dairy calves was investigated. Sixteen of the calves died acutely, without marked premonitory signs of disease. Four calves evaluated clinically had lethargy, pallor, weakness, tachycardia, tachypnea, and jugular venous
Diaphragm atrophy and contractile dysfunction in a murine model of pulmonary hypertension.
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Pulmonary hypertension (PH) causes loss of body weight and inspiratory (diaphragm) muscle dysfunction. A model of PH induced by drug (monocrotaline, MCT) has been extensively used in mice to examine the etiology of PH. However, it is unclear if PH induced by MCT in mice reproduces the loss of body
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