Mallery J A, Gardin J M, King S W, Ey S, Henry W L
Division of Cardiology, University of California Irvine, Orange 92668.
Chest. 1991 Aug;100(2):470-3. doi: 10.1378/chest.100.2.470.
Chronic pulmonary hypertension in humans is characterized by shortening of the pulmonary artery acceleration time as measured by Doppler echocardiography, such that the higher the pulmonary artery pressure, the shorter the pulmonary acceleration time. Increases in heart rate are also known to produce decreases in the pulmonary artery acceleration time. To explore the relationship between mean pulmonary artery pressure, heart rate, and Doppler pulmonary artery acceleration time, experimental acute pulmonary hypertension was created in nine Duroc swine, either by infusion of Sephadex beads with embolization of the pulmonary arterial circulation or by partially occluding the main pulmonary artery 8 to 10 cm distal to the pulmonic valve. Pulmonary artery Doppler flow velocity recordings and invasive pressure measurements were made at baseline and at paced atrial rates ranging from 60 to 160 beats per minute, in 20-beat increments. The results in this acute animal model reveal that increases in heart rate produced significant decreases in Doppler pulmonary artery acceleration time at mean pressures below 25 mm Hg. However, with mean pulmonary artery pressures greater than 25 mm Hg, both heart rate and increases in pulmonary artery pressure had no significant effect on acceleration time.
人类慢性肺动脉高压的特征是通过多普勒超声心动图测量的肺动脉加速时间缩短,即肺动脉压力越高,肺动脉加速时间越短。已知心率增加也会导致肺动脉加速时间缩短。为了探讨平均肺动脉压、心率和多普勒肺动脉加速时间之间的关系,对9头杜洛克猪进行实验性急性肺动脉高压建模,方法是注入葡聚糖珠栓塞肺动脉循环,或在肺动脉瓣远端8至10厘米处部分阻断主肺动脉。在基线以及心房起搏频率为每分钟60至160次(以20次为增量)时,进行肺动脉多普勒流速记录和有创压力测量。该急性动物模型的结果显示,在平均压力低于25毫米汞柱时,心率增加会导致多普勒肺动脉加速时间显著缩短。然而,当平均肺动脉压大于25毫米汞柱时,心率和肺动脉压力升高对加速时间均无显著影响。