PMID: 2498122Jun 1, 1989Paper

Comparative effects of isosorbide dinitrate, prednisolone, indomethacin, and elastase on the development of monocrotaline-induced pulmonary hypertension

Experimental and Molecular Pathology
T KatoM Kanisawa

Abstract

The pathogenesis of monocrotaline-induced pulmonary hypertension is not clear. Progressive pulmonary arteritis leading to vascular sclerosis, narrowing of the lumina, and thrombosis is the suspected sequence. To investigate this, we examined the effect of isosorbide dinitrate (ISDN), prednisolone, indomethacin, and elastase in 100 SD male rats, 4 weeks after the injection of monocrotaline (MCT) by cardiac catheterization, right ventricle-to-left ventricle plus septum weight ratio (RV/LV + S), histology, and electron microscopy. ISDN, a vasodilator, reduced the elevation of right ventricular (RV) pressure, RV/LV + S, and also pulmonary vascular remodeling; the characteristic histological feature was dilatation of small pulmonary arteries. Both prednisolone and indomethacin reduced RV pressure, RV/LV + S, and pulmonary vasculitis. Elastase, a protease which controls the metabolism of elastin in the arterial wall, likewise reduced RV pressure, RV/LV + S, and pulmonary vascular remodeling, with a significant decrease in elastosis of the small pulmonary arteries histologically. We concluded that all of the pathological processes resulting from arteritis are important in the development of MCT-induced pulmonary hypertension. In all e...Continue Reading

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Citations

Jun 22, 1991·Lancet·D I BoomsmaP Clark
Jan 1, 1990·Pharmacology & Therapeutics·R J Huxtable
Jun 1, 1996·Clinical and Experimental Pharmacology & Physiology·P R HuggardK M Summers
Jan 5, 2012·Chest·Laura C PriceMarc Humbert
Feb 2, 2013·Pulmonary Circulation·Mita DasJames West
Sep 15, 2009·American Journal of Physiology. Lung Cellular and Molecular Physiology·Kurt R StenmarkIvan F McMurtry

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