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1 Medicine-Pulmonary and Critical Care, Medical College of Wisconsin, Milwaukee, WI, USA; Research Service, Zablocki VA Medical Center, Milwaukee, WI, USA; Biomedical Engineering, Marquette University, Milwaukee, WI, USA
2 Biomedical Engineering, Marquette University, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: rmolthen{at}mcw.edu.
Little is known about the constituent hemodynamic consequences of structural changes, which 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 (SD) rats were removed, perfusion analysis 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 using volumetric micro-computed tomography (CT) and the arterial morphometry 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, SDH) or normoxia (21.0% O2, SDC) was performed. One metric, the normalized distensibility of the arteries, is significantly (p<0.001) larger [0.025 ± 0.0011(SE)/mmHg] (N = 9) in SDC rats compared to SDH [0.015 ± 0.00077 (SE)/mmHg] (N = 9). The results of the study show that these models can be applied to the SD rat data, and specifically, can be used to differentiate between the hypoxic and the control groups.
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