Krstic Anna Maria, Jones Timothy L M, Power Amelia S, Ward Marie-Louise
Department of Physiology, University of Auckland, Auckland 1142, New Zealand.
Division of Cardiology, Anschutz Medical Campus, University of Colorado, Aurora, CO 80045, USA.
Biomedicines. 2024 Aug 23;12(9):1944. doi: 10.3390/biomedicines12091944.
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.
肺动脉高压(PAH)的特征是肺血管阻力(PVR)增加,导致供应肺循环的肺动脉压力升高。右心室(RV)疾病通常是PAH对心脏右侧施加过大压力的结果。尽管PAH在人类中相对罕见,但持续PAH的影响很严重,即使是接受治疗的个体,预后也很差。随着PAH的发展,血流通过肺动脉受到限制,由于通过肺循环泵血的压力增加,右心室会发生肥大。随着时间的推移,RV肥大发展为右心衰竭,影响左心室的血液供应和体循环。尽管目前右心衰竭可以治疗,但无法治愈。因此,需要更多地研究在压力过载下导致心脏衰竭的生理变化。本综述旨在评估PAH的野百合碱(MCT)大鼠模型,作为研究与RV肥大和右心衰竭发展相关的细胞机制的一种手段。