Quantitative Models of the Rat Pulmonary Arterial Tree Morphometry Applied to Hypoxia-Induced Arterial Remodeling
Format of Original
American Physiological Society
Journal of Applied Physiology
Original Item ID
Little is known about the constituent hemodynamic consequences of structural changes that occur in the pulmonary arteries during the onset and progression of pulmonary arterial remodeling. Many disease processes are known to be responsible for vascular remodeling that leads to pulmonary arterial hypertension, cor pulmonale, and death. Histology has been the primary tool for evaluating pulmonary remodeling, but it does not provide information on intact vascular structure or the vessel mechanical properties. This study is an extension of our previous work in which we developed an alternative imaging technique to evaluate pulmonary arterial structure. The lungs from Sprague-Dawley rats were removed, perfusion analysis was performed on the isolated lungs, and then an X-ray contrast agent was used to fill the arterial network for imaging. The lungs were scanned over a range of intravascular pressures by volumetric micro-computed tomography, and the arterial morphometry was mapped and measured in the reconstructed isotropic volumes. A quantitative assessment of hemodynamic, structural, and biomechanical differences between rats exposed for 21 days to hypoxia (10% O2) or normoxia (21.0% O2) was performed. One metric, the normalized distensibility of the arteries, is significantly (P < 0.001) larger [0.025 ± 0.0011 (SE) mmHg−1] (n = 9) in normoxic rats compared with hypoxic [0.015 ± 0.00077 (SE) mmHg−1] (n = 9). The results of the study show that these models can be applied to the Sprague-Dawley rat data and, specifically, can be used to differentiate between the hypoxic and the control groups.
Molthen, Robert C.; Karau, Kelly L.; and Dawson, Christopher A., "Quantitative Models of the Rat Pulmonary Arterial Tree Morphometry Applied to Hypoxia-Induced Arterial Remodeling" (2004). Biomedical Engineering Faculty Research and Publications. 113.