作者: Tomoo Kato , Hajime Kitamura , Masayoshi Kanisawa
DOI: 10.1016/0014-4800(89)90040-3
关键词:
摘要: The pathogenesis of monocrotaline-induced pulmonary hypertension is not clear. Progressive arteritis leading to vascular sclerosis, narrowing the lumina, and thrombosis suspected sequence. To investigate this, we examined effect isosorbide dinitrate (ISDN), prednisolone, indomethacin, elastase in 100 SD male rats, 4 weeks after injection monocrotaline (MCT) by cardiac catheterization, right ventricle-to-left ventricle plus septum weight ratio (RV/LV + S), histology, electron microscopy. ISDN, a vasodilator, reduced elevation ventricular (RV) pressure, RV/LV S, also remodeling; characteristic histological feature was dilatation small arteries. Both prednisolone indomethacin RV vasculitis. Elastase, protease which controls metabolism elastin arterial wall, likewise remodeling, with significant decrease elastosis arteries histologically. We concluded that all pathological processes resulting from are important development MCT-induced hypertension. In experimental groups, decreased histopathologic changes correlated pressure. reduces suggested as new agent treat