An Analysis of the Pulsatile Hemodynamic Responses of the Pulmonary Circulation to Acute and Chronic Pulmonary Venous Hypertension in the Awake Dog
An Analysis of the Pulsatile Hemodynamic Responses of the Pulmonary Circulation to Acute and Chronic Pulmonary Venous Hypertension in the Awake Dog
复制标题
清醒狗肺循环对急慢性肺静脉高压的脉动血流动力学反应分析
作者：
R. Hopkins;J. Hammon;P. A. McHale;P. K. Smith;R. Anderson
在这项研究中，我们测量了高保真脉动压力和流量波形在入口处的肺血管床，以评估适应急性和慢性肺静脉高压清醒狗的差异。左心房压力（Pia）的急性升高是通过左心房球囊充气实现的，而慢性升高是通过将主动脉放置到左心房分流器来实现的。肺动脉液压阻抗计算和分析这些数据显示显着差异的反应急性和慢性左心房压力升高。急性应激犬（n = 12）肺血管阻力显著降低（Pla= 16.9 ± 1.0 mm Hg时，PVR = 212 ± 57 dynes sec/cm ~ 6; Pla= 28.6 ± 1.4 mm Hg时，PVR = 18 ± 115 dynes sec/cm ~ 6; = 6.1 ± 1.5 mm Hg，PVR = 355 ± 69 dynes sec/cm 5）和正常特征阻抗（Zo）（分别为210 ± 36、227 ± 39、178 ± 14 dynes sec/cm 5），表明小动脉-毛细血管灌注密度恢复，近端肺动脉物理特性无变化。慢性肺静脉高压组（n = 11）保留了正常的PVR（496 ± 30达因秒/厘米5），但表现出明显更高的特征阻抗，Zo = 361 ± 11达因秒/厘米5（P < 0.001）。这表明慢性静脉高血压对肺血管的物理性质具有可测量的不同和极其有效的影响，动脉硬度明显增加，与杨氏弹性模量增加4倍相关。这些变化不能被α-肾上腺素能阻滞或左心房压力的急性降低逆转。CircRes 47：902-910，1980
In this study we measured high fidelity pulsatile pressure and flow waveforms at the inlet to the pulmonary vascular bed to assess the differences in adaptation to acute and chronic pulmonary venous hypertension in awake dogs. Acute elevations in left atrial pressure (Pia) were effected by inflation of left atrial balloons, while chronic elevations were accomplished by placement of aorta to left atrial shunts. Pulmonary artery hydraulic impedance was calculated and analysis of these data revealed marked differences between the responses to acute and chronic elevations of left atrial pressure. The acutely stressed dogs (n = 12) had significantly decreased pulmonary vascular resistance (when Pla= 16.9 ± 1.0 mm Hg, PVR = 212 ± 57 dynes sec/cm5; when Pla= 28.6 ± 1.4 mm Hg, PVR = 18 ± 115 dynes sec/cm6; control Pi. = 6.1 ± 1.5 mm Hg, and PVR = 355 ± 69 dynes sec/cm5) and normal characteristic impedances (Zo) (210 ± 36, 227 ± 39, 178 ± 14 dynes sec/cm5, respectively), indicating recruitment of arteriolar-capillary perfusion density and no change in proximal pulmonary arterial physical properties. The chronic pulmonary venous hypertension group (n = 11) retained normal PVR (496 ± 30 dynes sec/cm5) but demonstrated a markedly higher characteristic impedance, Zo = 361 ± 11 dynes sec/cm5(P < 0.001). This indicated a measurably different and extremely potent effect of chronic venous hypertension on the physical properties of the pulmonary vessels with an apparently increased arterial stiffness correlating with a 4-fold increase in Young's elastic modulus. These changes were not reversed by α-adrenergic blockade or acute lowering of left atrial pressures. Circ Res 47: 902-910, 1980