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1 Department of Biomedical Engineering, University of Wisconsin, Madison, WI, USA
2 Department of Biostatistics and Medical Informatics, University of Wisconsin, Madison, WI, USA
* To whom correspondence should be addressed. E-mail: chesler{at}engr.wisc.edu.
Right heart failure due to pulmonary hypertension causes significant morbidity and mortality. To study the linked vascular mechanical and biological changes that are induced by pulmonary hypertension, we mechanically tested isolated left main pulmonary arteries from mice exposed to chronic hypobaric hypoxia and performed histological assays on contralateral vessels. In isolated vessel tests, hypoxic vessels stretched less in response to pressure than controls at all pressure levels. Given the short length and large diameter of the pulmonary artery, the tangent Young's modulus could not be measured; instead an effective elastic modulus was calculated, which increased significantly with hypoxia (280 ± 53 and 296 ± 50 kPa for 10 and 15 days, respectively versus 222 ± 35 kPa for control, p<0.02). Hypoxic vessels also had higher damping coefficients (0.063 ± 0.017 and 0.054 ± 0.014 for 10 and 15 days, respectively versus 0.033 ± 0.016 for control, p<0.002), indicating increased energy dissipation. The increased stiffness with hypoxia correlated with an increase in collagen thickness (percent collagen multiplied by wall thickness) as well as the sum of elastin and collagen thicknesses measured histologically in the artery wall. These results highlight the mechanobiological changes in the pulmonary vasculature that occur in response to hypoxia-induced pulmonary hypertension. Furthermore, they demonstrate significant vascular mechanical and biological changes that would increase pulmonary vascular impedance, leading to right heart failure.
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