Abstract 17109: Input Impedance Analysis of Pulmonary Hypertension Models Indicates That Monocrotaline and Sugen/hypoxia Induce Mechanically Different Vascular Remodeling
Introduction: Although complex pulmonary arterial remolding characterizes pulmonary hypertension (PH), the vascular mechanics has been evaluated by the static pressure-flow relationship (resistance, R) ignoring dynamic mechanical properties (compliance, C). We therefore evaluated pulmonary arterial input impedance (Z) capable of identifying not only resistance but also compliance in monocrotaline (MCT) and Sugen/Hypoxia (SuHx) PH models.
Methods: In 6 weeks Sprague-Dawley rats, we induced PH by the subcutaneous injection of MCT (60 mg/kg) or Sugen5416 (20 mg/kg) with 3 weeks hypoxia. In anesthetized PH rats, we measured pulmonary artery flow (PAF) and pressure (PAP) at 1000 Hz for 107.52 seconds under irregular pacing. We Fourier transformed both PAF and PAP to derive ensembled power spectra and crosspower spectra and taking their ratio yielded Z. We fitted the 2-element Windkessel model to Z and estimated R and C.
Results: MCT and SuHx significantly increased mean PAP (Control: 19.4±2.0, MCT: 31.3±4.0, SuHx: 39.4±6.5 mmHg, p<0.01) and shifted Z upward indicating the increased R (Control: 17.8±3.3, MCT: 71.4±16.3, SuHx: 81.8±18.4 mmHg/ml/sec, p<0.01). MCT and SuHx both decreased C (Control: 2.6±0.4, MCT: 1.5±0.6, SuHx: 0.9±0.2 х10-3ml/mmHg, p<0.01). However, the time constant was higher in MCT than in SuHx (Control: 90.7±8.6, MCT: 130.0±21.5, SuHx: 92.6±2.0 msec, p<0.05) (Figure). MCT predominantly remodeled resistance vessels while SuHx remodeled both resistance and compliance vessels.
Conclusions: We conclude that the impedance analysis is capable of characterizing how remodeling affects vascular mechanical properties, which are not identifiable if we analyze resistance alone. Hence the impedance analysis is applicable in patients, it may serve as a new tool in functionally analyzing vascular remodeling in PH patients.
Author Disclosures: T. Nishikawa: None. K. Saku: None. T. Sakamoto: None. Y. Murayama: None. T. Kishi: None. K. Sunagawa: None.
- © 2015 by American Heart Association, Inc.