Background: Pulmonary artery (PA) impedance provides detailed information on right ventricular (RV) afterload in pulmonary hypertension (PH). This study aimed to examine PA impedance in a rat model of monocrotaline-induced PH (MCT-PH) and to develop an experimental system for in vivo loading of pathological PA impedance on the RV of normal rats. Methods and Results: PA impedance was quantified in normal (n = 10) and MCT-PH rats (n = 10) using a three-element Windkessel (3-WK) model. Compared to normal rats, MCT-PH rats had higher characteristic impedance (ZC) and peripheral pulmonary resistance (RP) (ZC: 0.121 ± 0.039 vs 0.053 ± 0.167 mmHg·min/ml, P < 0.001; RP: 0.581 ± 0.334 vs 0.252 ± 0.105 mmHg·min/ml, P = 0.013) and lower pulmonary artery compliance (CP) (0.242 ± 0.131 vs 0.700 ± 0.186 ml/mmHg, P < 0.001). In another 10 normal rats, a computer-controlled servo pump was connected to the left PA for loading PA impedance with parameters in pathological ranges designed by the 3-WK model. Activation of the servo pump decreased the error of measured versus target PA impedance (modulus: from 0.047 ± 0.020 without pump activation to 0.019 ± 0.007 mmHg·min/ml with pump activation, P < 0.001; phase: 0.085 ± 0.028 to 0.043 ± 0.012 radians, P < 0.001). Conclusions: MCT-PH increases ZC and RP and decreases CP. Our servo pump system, which is capable of imposing arbitrary PA impedance with pathological parameters may offer a unique opportunity to delineate the pathological significance of PA impedance in PH.
- pulmonary hypertension
- pulmonary artery impedance
- Windkessel model
- Copyright © 2015, American Journal of Physiology - Heart and Circulatory Physiology