Abstract
Pulmonary arterial hypertension (PAH) is a syndrome characterized by pulmonary vascular remodeling and vasoconstriction, leading to increased pulmonary vascular resistance, right ventricular pressure overload and, eventually, to right ventricular failure and premature death. Animal models have been an essential tool for understanding pulmonary hypertension pathophysiology and for the discovery and development of novel therapies.
MCT-induced PAH in rats leads to a significant increase in RV pressure and pulmonary vascular remodeling, as well as greater RV hypertrophy. In this chapter, we describe protocols for inducing and assessing the monocrotaline (MCT) rat model, the most classical and widely used in vivo model of PAH. Using this protocol, rats reproducibly develop pulmonary hypertension with a mean pulmonary pressure of ~40 mmHg approximately 4 weeks after single MCT administration.
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Acknowledgments
This work was supported by grants from the National Institutes of Health R01HL133554 to L.H, from the American Heart Association (AHA-17SDG33370112) to Y.S., and from the R01 HL117505, HL 119046, HL129814, 128072, HL131404, R01HL135093, a P50 HL112324, and two Transatlantic Fondation Leducq grants (R.J.H.). We would like to acknowledge the Gene Therapy Resource Program (GTRP) of the National Heart, Lung, and Blood Institute, National Institutes of Health.
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Bueno-Beti, C., Sassi, Y., Hajjar, R.J., Hadri, L. (2018). Pulmonary Artery Hypertension Model in Rats by Monocrotaline Administration. In: Ishikawa, K. (eds) Experimental Models of Cardiovascular Diseases. Methods in Molecular Biology, vol 1816. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4939-8597-5_18
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DOI: https://doi.org/10.1007/978-1-4939-8597-5_18
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