Vascular Mechanics in Decellularized Aortas and Coronary Resistance Microvessels in Type 2 Diabetic db/db Mice
Document Type
Article
Publication Date
2015
Abstract
We previously reported differences in stiffness between macro- and micro-vessels in type 2 diabetes (T2DM). The aim of this study was to define the mechanical properties of the ECM independent of vascular cells in coronary resistance micro-vessels (CRMs) and macro-vessels (aorta) in control Db/db and T2DM db/db mice. Passive vascular remodeling and mechanics were measured in both intact and decellularized CRMs and aortas from 0 to 125 mmHg. We observed no differences in intact control and diabetic aortic diameters, wall thicknesses, or stiffnesses (p > 0.05). Aortic decellularization caused a significant increase in internal and external diameters and incremental modulus over a range of pressures that occurred to a similar degree in T2DM. Differences in aortic diameters due to decellularization occurred at lower pressures (0–75 mmHg) and converged with intact aortas at higher, physiological pressures (100–125 mmHg). In contrast, CRM decellularization caused increased internal diameter and incremental modulus only in the db/db mice, but unlike the aorta, the intact and decellularized CRM curves were more parallel. These data suggest that (1) micro-vessels may be more sensitive to early adverse consequences of diabetes than macro-vessels and (2) the ECM is a structural limit in aortas, but not CRMs. © 2015 Biomedical Engineering Society
Publication Title
Annals of Biomedical Engineering
Recommended Citation
Anghelescu, Mircea; Tonniges, J.; Calomeni, E.; Shamhart, P. E.; Agarwal, G.; Gooch, K. J.; and Trask, A. J., "Vascular Mechanics in Decellularized Aortas and Coronary Resistance Microvessels in Type 2 Diabetic db/db Mice" (2015). PCOM Scholarly Works. 1521.
https://digitalcommons.pcom.edu/scholarly_papers/1521
Comments
This article was published in Annals of Biomedical Engineering .
The published version is available at http://dx.doi.org/10.1007/s10439-015-1333-4.Copyright © 2015.