摘要
本文通过静脉持续滴注血检素A2类似体U46619复制急性肺动脉高压实验模型，借助右心导管技术和利用压力波形面积确定动脉顺应性的改进方法，评价急性肺动脉高压状态下的肺血管力学特性。实验结果发现，当平均肺动脉压从2.60±0．3kPa上升至3.75±0.45kPa后；心排量（CO）无显著性变化（1．85±0．21vs1．21±0．25l／min；P＞0.05），而肺小动脉血管阻力（PVR）明显升高（31.4±9．4vs148．7±12．3kPa·s／L，P＜0．01）与肺动脉平均压相对应的血管顺应性Cm显著降低（12．43±2．62vs10．30±3．12ml／kPa，P＜0．05），而反映肺血管壁固有结构特性的零压顺应性Co无明显改变（15.22±2.98vs14.31±3.49ml／kPa，P＞0．05。本实验提示，在急性肺高压状态，肺小动脉收缩引起的肺血管阻力变化是关键因素，选择治疗急性肺高压的扩血管药物应偏重于主要作用于小动脉血管的药物。
In this paper, we studledthe mechanical properties of canine pulmonary arterles under acute pulmonary hypertenslon. The condltion was induced by infusion of the thromboxane A2 analogue U46619 using right heart catheterization techniques. The theoretical study was based a Windkessel Model. The results demonstrated a mlnimal difference of cardiac output (CO) (1.85- 0.21 vs 1.21 - 0.25 lml, P0.05) before and after the induced condition of acute pulmonary hypertension.However the results showed a significantly!ffle in pulmonary vessel resistance (PVR) under the induced condition as compared with the normal situation (31.4- 9.4 vs 148.7 12.3kPa s/L,P<0.01). As of the pulmonary arterlal compliance, Cm decreased noticeably (12.43 - 2.62 vs 10.30 - 3.12ml/kPa, P<0.05), while Co had only negligible variation. These results suggested that the change of PVR caused by small pulmonary artery contraction was a main factor influencing the acute pulmonary hypertension, therefore, the vasodi1ator which dilate small arterles was the optimal cholce in treating acute pulmonary hypertension.
出处
《医用生物力学》
EI
CAS
CSCD
1998年第1期25-29,共5页
Journal of Medical Biomechanics
关键词
急性
肺动脉高压
肺小动脉
血管阻力
Acute Pulmonary
Hypertension Pulmonary Arterial Compliance Pulmonary Vessel Resistance
