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1 Department of Mechanical Engineering, Temple University, Philadelphia, PA, USA; Department of Biomedical Engineering, University of Tennessee, Health science center, Memphis, TN, USA
2 Division of Cardiovascular Diseases, University of Tennessee, Health science center, Memphis, TN, USA
3 Division of Rheumatology, University of Tennessee, Health science center, Memphis, TN, USA
4 Department of Mechanical Engineering, Temple University, Philadelphia, PA, USA; Department of Radiation Oncolgy, Temple University, Phiadelphia, PA, USA; Department of Biomedical Engineering, University of Tennessee, Health science center, Memphis, TN, USA
* To whom correspondence should be addressed. E-mail: mkiani{at}temple.edu.
A series of novel techniques, adapted from the field of tumor biology, were developed to quantify vascular structure and function and to explore the role of AngII receptor AT1 in cardiac remodeling post-MI. We examined the scar neovasculature at 1-4 weeks post-MI in Sprague-Dawley rats with a view towards its ability to deliver and exchange oxygen. CD31 and DiOC7(3) staining was used to respectively visualize anatomical vessels vs. those perfused. EF5/Cy3 immunohistochemical staining was used to quantify tissue hypoxia. We compared untreated controls with rats treated with losartan, an AT1 receptor antagonist. Our findings indicated that at the infarct site there was not only a 42-75% (1-4 weeks post-MI, respectively) decrease in the number of anatomical vessels compared to controls, but also a decrease in the fraction of perfused vessels from 70% in normal coronary vasculature to 48% at the infarct site. These changes were accompanied by progressive increases in diffusion distance and tissue hypoxia (100% increase in EF5/Cy3 staining at 4 weeks post-MI). Losartan treated rats exhibited a significantly less marked reduction in vascular perfusion and significantly lesser extent of tissue hypoxia. Over the course of 4 weeks post-MI, there is a reduction in coronary vasculature at the infarct site, the extent of which is attenuated by losartan. These findings implicate AT1 receptor upregulation, and perhaps angiotensin related peptides, as being antiangiogenic.
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