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Rajvinder Kaur*, A. N. Kalia, Saurabh Sharma, Jhilika Singh and Dipanshu Panday


Pulmonary arterial hypertension (PAH), is highly ruinous condition that targets the endothelial cells of pulmonary arteries resulting in vasoconstriction and vascular remodeling which has become rampant and perpetuating. Pulmonary hypertension is also a predictor of various adverse effects. Subsequently, preclinical experimental settings are organized to investigate the PAH in animal models and new strategies for patient with PAH are needed. The pathogenesis of the disease is poorly understood due to its complicated structure. Animal models have improved current understanding of the complex pathophysiology of the disease and contributed to understand its underlying mechanisms which help in the development of therapeutic targets. Chronic hypoxia and the monocrotaline-induced rat models are the most widely used animal models of pulmonary arterial hypertension. It is amazing that rodent models, such as monocrotaline and pneumonectomy and left pneumonectomy plus Su5416 yield more severe PH than single stimuli models which is similar to human pathophysiology. There are also new models such as endothelin B receptor deficiency, bleomycin induced pulmonary hypertension and some other models are used which are based on endothelial cell proliferation due to some growth factors. Ren2 model is also a new model which is based on renin angiotensin system. However the cumulative literature for animal models for pulmonary hypertension is inadequately available. In the present review, we have discussed various experimental models of pulmonary hypertension.

Keywords: Pulmonary hypertension; chronic hypoxia; endothelium dysfunction; vascular remodeling; rat models; Vascular remodeling.

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