monocrotaline/acidente vascular cerebral

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Right ventricular end-diastolic stiffness heralds right ventricular failure in monocrotaline-induced pulmonary hypertension.

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Recent studies suggest right ventricular (RV) stiffness is important in pulmonary hypertension (PH) prognosis. Smaller stroke volume (SV) variation after a certain RV end-diastolic pressure (EDP) respiratory variation as assessed by spectral transfer function (STF) may identify RV stiffness. Our aim

Alterations in pharmacological action of the right ventricle of monocrotaline-induced pulmonary hypertensive rats.

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The present study was undertaken to elucidate pathophysiological and pharmacological alterations in the right ventricle in monocrotaline-administered (MCT) rats. Examination of tissue weights of the MCT and age-matched control (CON) rats indicated the right ventricular (RV) hypertrophy until 8 weeks

Fasudil reduces monocrotaline-induced pulmonary arterial hypertension: comparison with bosentan and sildenafil.

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Pulmonary arterial hypertension (PAH) still cannot be cured, warranting the search for novel treatments. Fasudil (a Rho kinase inhibitor) was compared with bosentan (an endothelin receptor blocker) and sildenafil (a phosphodiesterase 5 inhibitor), with emphasis on right ventricular (RV) function, in

Compensated right ventricular function of the onset of pulmonary hypertension in a rat model depends on chamber remodeling and contractile augmentation.

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Right-ventricular function is a good indicator of pulmonary arterial hypertension (PAH) prognosis; however, how the right ventricle (RV) adapts to the pressure overload is not well understood. Here, we aimed at characterizing the time course of RV early remodeling and discriminate the contribution

Determination of the effects of pulmonary arterial hypertension and therapy on the cardiovascular system of rats by impedance cardiography.

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OBJECTIVE To evaluate the effects of bosentan, sildenafil, and combined therapy on the cardiovascular system using impedance cardiography (ICG) in rats with monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH). METHODS Seventy male Wistar-albino rats were randomized into five groups. A

The phenomena of mechanical interaction of segments of hypertrophied myocardium.

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The main aims of adaptation mechanisms of heart contractility are to regulate the stroke volume and optimize the global heart function. These mechanisms manifest themselves in hearts of healthy animals and in hearts with severe hypertrophy in different ways. Severe right ventricle hypertrophy was

Iloprost improves ventricular function in the hypertrophic and functionally impaired right heart by direct stimulation.

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Right heart function is an important predictor of morbidity and mortality in patients suffering from pulmonary arterial hypertension and congenital heart diseases. We investigated whether the prostacyclin analog iloprost has a direct inotropic effect in the pressure-overloaded hypertrophic and

Hemodynamic and inotropic effects of milrinone after heart transplantation in the setting of recipient pulmonary hypertension.

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BACKGROUND Right ventricular failure remains an important cause of early morbidity and death after heart transplantation and is commonly related to preexistent recipient chronic pulmonary hypertension, which occurs as a result of long-standing congestive heart failure. In this study, the hemodynamic

Molecular and functional mechanisms of right ventricular adaptation in chronic pulmonary hypertension.

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BACKGROUND Chronic pulmonary hypertension can lead to compensatory changes in the right ventricle. In this study, the adaptive mechanisms of the right ventricle in the setting of pulmonary hypertension were assessed at the molecular and functional level using a canine model of monocrotaline

Effects of nitric oxide after cardiac transplantation in the setting of recipient pulmonary hypertension.

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BACKGROUND Recipient pulmonary hypertension secondary to chronic congestive heart failure is a significant risk factor for right ventricular failure after cardiac transplantation. In this study, the hemodynamic and inotropic effects of nitric oxide (NO) were examined after bicaval cardiac

Right ventricular adaptation to increased afterload after orthotopic cardiac transplantation in the setting of recipient chronic pulmonary hypertension.

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BACKGROUND Right ventricular (RV) failure remains an important risk factor for early morbidity and mortality after orthotopic cardiac transplantation and is most commonly related to preexistent chronic pulmonary hypertension (CPH) in the recipient, which occurs secondary to long-standing congestive

Right ventricular dysfunction after cardiac transplantation: primarily related to status of donor heart.

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BACKGROUND It is unclear whether right ventricular dysfunction after transplantation is due to donor brain death-related myocardial injury or recipient pulmonary hypertension. METHODS A canine donor model of brain death and a monocrotaline pyrrole-induced chronic pulmonary hypertension recipient

Lipopolysaccharide acutely suppresses right-ventricular strain in rats with pulmonary artery hypertension.

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Worsening right ventricular (RV) dysfunction in the presence of pulmonary artery hypertension (PAH) increases morbidity and mortality in this patient population. Transthoracic echocardiography (TTE) is a non-invasive modality to evaluate RV function over time. Using a monocrotaline-induced PAH rat

Haemodynamic studies in veno-occlusive disease of the liver.

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Haemodynamic studies in 8 tribal patients from central India with veno-occlusive disease of the liver are reported. The disease was caused by eating cereals contaminated with seeds of a crotalaria species rich in toxic pyrrolizidine alkaloids similar to monocrotaline and fulvine. All patients showed

Acute effects of levosimendan in experimental models of right ventricular hypertrophy and failure.

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Pulmonary arterial hypertension (PAH) is a fatal disease, and the ultimate cause of death is right ventricular (RV) failure. In this study, we investigated the acute hemodynamic effects of levosimendan in two rat models of RV hypertrophy and failure. Wistar rats were randomized to receive sham

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