Inhibition of rho kinase attenuates high flow induced pulmonary hypertension in rats.

摘要: Background The RhoA/Rho kinase pathway may participate in the pathogenesis of hypoxia and monocrotaline induced pulmonary hypertension. This study tested whether is involved high flow hypertension rats. Methods Male Wistar rats (4 weeks) were randomly divided into 4 shunt groups, treated groups control groups. Shunt underwent left common carotid artery/external jugular vein operation. Control sham Treated received fasudil treatment others same dose saline. At weeks 1, 2, 8 study, right ventricular systolic pressure was measured blood gases analysed to calculate Qp/Qs. weight ratio ventricle plus septum mean percentage medial wall thickness moderate sized arteries obtained. RhoA activity detected using Rho assay reagent. quantified by extent MYPT1 phosphorylation with Western blot. Proliferating cells evaluated proliferating cell nuclear antigen immunohistological staining. Results Carotid artery/jugular resulted flow, both an acute a chronic elevation pressure, significant thickening characterized smooth muscle proliferation, hypertrophy increased activation kinase. Fasudil lowered artery suppressed attenuated inhibited together suppression but not activity. Conclusions Activated associated vasoconstriction remodelling could improve inhibiting