Abstract 19492: Novel Assessment of Pulmonary and Systemic Pressures During Treadmill Testing via Implantable Telemetry in a Rat Model of Pulmonary Arterial Hypertension
Objectives: 1) To determine if pulmonary arterial pressures (PAP) may be measured simultaneously with systemic blood pressures (BP) during exercise testing in laboratory rats using implantable telemetry; and 2) To determine the relationship of exercise intensity to acute PAP exercise responses over the course of PAH development.
Methods: A specialized implantable transmitter (Data Sciences International); via telemetry following thoracotomy with right ventricular (RV) and abdominal aortic catheter positioning, respectively enabled simultaneous systolic, diastolic and mean PAP and BP recordings. Following recovery, an incremental treadmill test measured maximal aerobic capacity (VO2max) via analysis of expired gases. Steady state exercise testing was then performed for 3 different submaximal relative intensities: 50, 75, and 90% VO2max. Pressures were recorded during each test, as well as pre- and post- exercise. At 2.5 weeks following monocrotaline (MCT, 40 mg/kg) administration (mild PH) and 7 weeks post-MCT (advanced PH), VO2max and steady-state exercise tests were repeated.
Results: Compared to pre-MCT, at 2.5 weeks post-MCT systolic PAP increased from 25 to 41 mmHg at rest; from 105 to 117 mmHg at peak exercise; and from 40 to 58 mmHg, 46 to 65 mmHg, and 55 to 75 mmHg during running at 50, 75, and 90% VO2max, respectively. At 7 weeks post-MCT, PAP further increased at rest (to 59 mmHg), and during steady state running (to 69, 70, and 73 mmHg, at 50, 75, and 90% VO2max, respectively). During recovery from steady state exercise, the fall in PAP occurred more rapidly post-MCT, bringing PAP to even lower than resting from 10 min to 2h into recovery.
Conclusions: Using implantable telemetry we have accomplished dual pressure recordings during serial exercise tests before and after PAH induction. The rise in PAP relative to exercise intensity is steeper in PAH but is accompanied by a post-exercise window of normalized PAP, which may be attributed to pronounced acute pulmonary endothelial activation. Future work will investigate how these acute effects translate to wall stress and RV remodeling with chronic exercise training and may allow for optimized exercise prescription for patients affected with PAH.
Author Disclosures: A. Zinn: None. R. Novack: None. A. Fisher: None. R. Presson: None. D. Zaretsky: None. D. Rusyniak: None. T. Lahm: None. M. Brown: None.
This research has received full or partial funding support from the American Heart Association
- © 2014 by American Heart Association, Inc.