Affiliation:
1. Department of Artificial Organ Medicine, Faculty of Medicine, Osaka University Graduate School of Medicine, Osaka, Japan;
2. Department of Cardiovascular Dynamics, National Cerebral and Cardiovascular Center, Osaka, Japan
Abstract
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. PA impedance was quantified in normal ( n = 10) and MCT-PH rats ( n = 10) using a three-element Windkessel (3-WK) model. Compared with normal rats, MCT-PH rats had higher characteristic impedance ( ZC) and peripheral pulmonary resistance ( RP) ( ZC: 0.121 ± 0.039 vs. 0.053 ± 0.017 mmHg·min·ml−1, P < 0.001; RP: 0.581 ± 0.334 vs. 0.252 ± 0.105 mmHg·min·ml−1, 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 group of 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 vs. target PA impedance (modulus: from 0.047 ± 0.020 without pump activation to 0.019 ± 0.007 with pump activation, P < 0.001; phase: 0.085 ± 0.028 to 0.043 ± 0.012 radians, P < 0.001). In conclusion, MCT-PH increases ZCand RPand 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.
Publisher
American Physiological Society
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology
Cited by
5 articles.
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