This study investigated the effects of angiotensin II (AngII) intervention, using captopril and losartan, on the expression of matrix metalloproteinase-2 (MMP-2), MMP-9, tissue inhibitor of metalloproteinase-1 (TIMP-1), and collagen in rats with pulmonary hypertension, in an effort to understand mechanisms underlying pulmonary vascular remodeling. A total of 40 male Sprague-Dawley rats were randomly divided into normal group, model group, captopril group, and losartan group.
The aim of this study was to investigate the correlation between circulating endothelial progenitor cell (EPC) levels and plasma prostacyclin (PGI2) concentrations in pulmonary hypertension (PH) rat models. Monocrotaline was used to induce PH, and the number of CD34/Flk-1-double-positive mononuclear cells in peripheral CD45-negative blood was counted by flow cytometry, which reflected EPC circulation. The Greiss method was used to detect the plasma PGI2 concentration. Simple linear regression analysis was used to analyze the relationship between EPC and PGI2.
Pulmonary hypertension (PH) secondary to chronic kidney disease (CKD) is common, but in stages 1-3 CKD patients, it remains unclear. We sought to evaluate the prevalence of PH and elucidate the possible pathogenesis in Chinese patients with early stage kidney disease. Doppler-estimated pulmonary systolic artery pressure (PASP) was measured in 101 CKD patients with glomerular filtration rate (GFR) ≥60 mL/min/1.73 m2 and 27 CKD patients with GFR 2. Echocardiographic parameters, plasma brain natriuretic peptide (BNP), and baseline characteristics of patients were recorded.