摘要
在大鼠实验性慢性缺氧期间,长期喂服硝苯吡啶使缺氧所致的右室肥厚减轻。肺动脉内注射硝苯吡啶后,缺氧大鼠肺动脉收缩压呈三相性变化,早期迅速升高、中期缓慢升高及晚期逐渐下降;降低,右室心肌力学指标+dp/dt_(max)及|-dp/dt_(max)|升高,t-dp/dt_(max)缩短;右室舒张压及舒张末压降低。口服或肺动脉内给药对颈动脉压及心率无明显影响。
Myocardial contractility and pulmonary hypertension in hypoxic Wistar rats were studied and results compared with normal control and hypoxic rats treated with nifedipine.After living in hypobaric oxygen chamber for 10 days pulmonary arterial pressure (PAP), right ventricular end diastolic pressure (RVEDP), weight of right ventricle (RV) and hematocrit (Ht) of the rats were increased significantly with increase of dp/dtmax and decrease of t dp/dtmax.In group of hypoxia with oral nifedipine, increase of PAP.Ht, RVEDP and + dp/dtmax were similar with that of hypoeic rats excspt for signifi cant decrease of weight of RV.After injection of nifedipine into pulmonary artery,a triphasic increase of pulmonary arterial pressure(PAPs)in all 3 groups was found: 1) phase 0 ,a sharp rise of PAPs with a slight decrease of PAPd within 1 min; 2) phase 1, a slow tise of PAPs with a gradual decrease of PAPd in 1-5 min and 3) phase 2, (recovery phase), a gradual return of PAP to normal 5 min later. As to myocardial contractility of RV, increase of + dp/dtmax and decreases of t-dp/dtmax, RVDP and RVEDP were noticed after injection.Nifedipine did not change systemic pressure and heart rate of rats in our study.
出处
《中国医学科学院学报》
CAS
1987年第2期99-104,共6页
Acta Academiae Medicinae Sinicae
关键词
缺氧
肺动脉高压
心室肥厚
血液动力学
心肌力学
hypoxia pulmonary hypertension myocardial hypertrophy hemodynamics contractility hematocrit