This review evaluates the monocrotaline rat model of pulmonary artery hypertension for studying cellular mechanisms of right ventricular hypertrophy and right heart failure.
This review evaluates the monocrotaline rat model as a means to study cellular mechanisms of right ventricular hypertrophy and right heart failure in pulmonary artery hypertension.
Pulmonary artery hypertension (PAH) is characterised by increased pulmonary vascular resistance (PVR) resulting in elevated pressure in the pulmonary artery supplying the pulmonary circulation. Disease of the right ventricle (RV) often manifests as a result of PAH placing excessive pressure on the right side of the heart. Although a relatively rare disease in humans, the impact of sustained PAH is severe, with poor outcomes even in treated individuals. As PAH develops, the blood flow is restricted through the pulmonary arteries and the right ventricle hypertrophies due to the increased strain of pumping blood through the pulmonary circulation. With time, RV hypertrophy progresses to right heart failure, impacting the supply of blood to the left ventricle and systemic circulation. Although right heart failure can currently be treated, it cannot be cured. There is therefore a need for more research into the physiological changes that cause the heart to fail under pressure overload. This review aims to evaluate the monocrotaline (MCT) rat model of PAH as a means of studying the cellular mechanisms associated with the development of RV hypertrophy and right heart failure.
Krstic et al. (Fri,) conducted a review in Pulmonary artery hypertension and right heart failure. Monocrotaline (MCT) rat model was evaluated. This review evaluates the monocrotaline rat model of pulmonary artery hypertension for studying cellular mechanisms of right ventricular hypertrophy and right heart failure.