摘要
目的:利用测定血浆内皮素-1(ET-1)水平来探讨卡托普利对野百合碱(MCT)诱发肺心病肺动脉高压的作用机制。方法:将33只雄性Wister大鼠随机分为正常对照组(N组)、肺心病模型组(M组)、卡托普利组(CPT组),每组11只。予MCT(50mg/kg)腹腔内注射复制大鼠肺心病模型后,分别给CPT组及N组大鼠连续灌胃卡托普利(25mg·kg-1·d-1)和等量生理盐水21d。采用改良右心导管术测定肺血流动力学参数,以非平衡法测定血浆ET-1水平;处死大鼠后,称量肺湿重(wW)、右心室自由壁(RV)和左心室加室间隔(LV+S)重,计算右心肥厚指数(RV/LV+S)。结果:卡托普利能明显降低肺心病模型大鼠的平均肺动脉压、wW及血浆ET-1水平(P<0.05,或P<0.01),轻微抑制RV/LV+S的增加(P>0.05)。结论:长期使用卡托普利能有效降低MCT所致肺心病肺动脉高压,改善心功能,其作用机制可能与显著降低血浆ET-1水平有关。
Objective: To investigate the mechanism and the effect of captopril on experimental cor pulmonale by means of measuring the level of plasma endothelin-1. Methods: Adult male Wister rats were given a single dose of monocrotaline(50mg/kg) to induce the model of cor pulmonale. 33 cases were randomly divided into normal control group, model group and captopril treatment group(n=11). Then they were treated with gastric infusion of normal saline、captopril respectively for 21 days. The parameters of pulmonary hemodynamics were monitored by Gould 3400 polygraph system through the cannulation of polyvinyl tube. Right ventricle to left ventricle plus interventricular septum weight ratio, and the wet weight of lung were measured. The level of plasma endothelin-1 was determined by the method of nonequilibrium. Results: Captopril significantly inhibited the progression of pulmonary artery pressure(P<0.01). It decreased the right heart hypertrophy index, and reduced the wet weight of lung and the level of plasma endothelin-1(P<0.05,or P<0.01). Conclusions: Captopril is able to reduce the pulmonary hypertension and improved the heart function. Its mechanisms may be related to reducing the level of plasma endothelin-1.
出处
《泸州医学院学报》
2005年第3期208-211,共4页
Journal of Luzhou Medical College