Department of Respiratory Medicine, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, China.
Cardiac Arrhythmia Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Clin Hemorheol Microcirc. 2020;74(2):189-200. doi: 10.3233/CH-190668.
Drag-reducing polymers (DRPs) was previously demonstrated to increase blood flow, tissue perfusion, and reduce vascular resistance. The purpose of this study was to investigate the effect of DRPs on pulmonary vascular remodeling and right ventricular dysfunction in a rat model of chronic hypoxia-induced pulmonary hypertension (HPH). A total of forty male Wistar rats were randomly and equally assigned into four experimental groups (Group I: normoxia + saline, Group II: normoxia + PEO, Group III: hypoxia + saline, Group IV: hypoxia + PEO) and maintained in normoxia (21% O2) or hypobaric hypoxia (10% O2). After four weeks, comparisons were made of the following aspects: the mean pulmonary arterial pressure (mPAP), right ventricular systolic pressure (RVSP), right ventricular hypertrophy, wall thickness of pulmonary trunk and arteries, internal diameter of pulmonary arteries, cardiomyocyte cross-sectional area (CM CSA), and ultrastructure of right ventricular. Treatment with PEO in Group IV attenuated the increases in RVSP and mPAP (40.5±7.2 and 34.7±7.0 mmHg, respectively, both P < 0.05), compared with Group III. Distal vascular remodeling was visible as a significant increase in medial wall thickness (64.2±12.3% vs. 43.95±7.0%, P < 0.01) and a remarkable decrease in internal diameter of small pulmonary arteries (35.2±9.7μ m vs. 50.4±14.7μ m, P < 0.01) in Group III, to a greater extent than that detected in Group IV. Nevertheless, no significant histopathological differences in medial wall thickness was observed in pulmonary trunk between Group III and Group IV (P > 0.05), denoting that PEO chiefly attenuated the remodeling of small pulmonary arteries rather than main arteries in hypoxic environment. Infusion of DRPs (intravenous injection twice weekly) also attenuated the index of right ventricular hypertrophy, protected against the increase of cardiomyocyte cross-sectional area, and provided protection for cardiac ultrastructure. DRP treatment with intravenous injection elicited a protective effect against pulmonary vascular remodeling and right ventricular dysfunction in the rat model of HPH. DRPs may offer a new potential approach for the treatment of HPH, which may have theoretical significance and application value to society.
减阻聚合物（DRPs）先前已被证明可增加血流量、组织灌注并降低血管阻力。本研究旨在探讨 DRPs 对慢性缺氧诱导肺动脉高压（HPH）大鼠模型中肺血管重塑和右心室功能障碍的影响。总共 40 只雄性 Wistar 大鼠被随机平均分为四组实验（I 组：常氧+生理盐水，II 组：常氧+PEO，III 组：缺氧+生理盐水，IV 组：缺氧+PEO），并分别维持在常氧（21% O2）或低压缺氧（10% O2）环境中。四周后，比较以下方面：平均肺动脉压（mPAP）、右心室收缩压（RVSP）、右心室肥厚、肺动脉干和动脉壁厚度、肺动脉内径、心肌细胞横截面积（CM CSA）和右心室超微结构。与 III 组相比，IV 组 PEO 治疗可减轻 RVSP 和 mPAP 的升高（分别为 40.5±7.2 和 34.7±7.0mmHg，均 P<0.05）。远端血管重塑表现为中膜壁厚度显著增加（64.2±12.3%比 43.95±7.0%，P<0.01）和小肺动脉内径明显减小（35.2±9.7μm 比 50.4±14.7μm，P<0.01），程度大于 IV 组。然而，III 组和 IV 组之间肺动脉干中膜壁厚度无显著的组织病理学差异（P>0.05），表明 PEO 主要减轻了低氧环境中小肺动脉的重塑，而不是主肺动脉的重塑。DRPs（每周静脉注射两次）的输注也可减轻右心室肥厚指数，防止心肌细胞横截面积增加，并为心脏超微结构提供保护。静脉注射 DRP 对 HPH 大鼠模型中的肺血管重塑和右心室功能障碍具有保护作用。DRPs 可能为 HPH 的治疗提供一种新的潜在方法，这对社会具有理论意义和应用价值。
