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2型糖尿病db/db小鼠脱细胞主动脉和冠状动脉阻力微血管的血管力学

Vascular Mechanics in Decellularized Aortas and Coronary Resistance Microvessels in Type 2 Diabetic db/db Mice.

作者信息

Anghelescu Mircea, Tonniges Jeffrey R, Calomeni Ed, Shamhart Patricia E, Agarwal Gunjan, Gooch Keith J, Trask Aaron J

机构信息

Department of Biological and Allied Health Sciences, Ohio Northern University College of Arts & Sciences, Ada, OH, USA.

Biophysics Graduate Program, Davis Heart and Lung Research Institute, The Ohio State University College of Arts and Sciences, Columbus, OH, USA.

出版信息

Ann Biomed Eng. 2015 Nov;43(11):2760-70. doi: 10.1007/s10439-015-1333-4. Epub 2015 May 19.

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.

摘要

我们之前报道过2型糖尿病(T2DM)中微血管和大血管之间的硬度差异。本研究的目的是确定对照Db/db和T2DM db/db小鼠冠状动脉阻力微血管(CRM)和大血管(主动脉)中独立于血管细胞的细胞外基质(ECM)的力学特性。在完整和脱细胞的CRM和主动脉中,测量了0至125 mmHg范围内的被动血管重塑和力学性能。我们观察到完整的对照和糖尿病主动脉直径、壁厚或硬度没有差异(p>0.05)。主动脉脱细胞导致内径和外径以及增量模量在一定压力范围内显著增加,在T2DM中也出现了类似程度的增加。由于脱细胞导致的主动脉直径差异在较低压力(0-75 mmHg)时出现,并在较高的生理压力(100-125 mmHg)时与完整主动脉趋于一致。相比之下,CRM脱细胞仅在db/db小鼠中导致内径和增量模量增加,但与主动脉不同,完整和脱细胞的CRM曲线更平行。这些数据表明:(1)微血管可能比大血管对糖尿病的早期不良后果更敏感;(2)ECM是主动脉的结构限制因素,但不是CRM的结构限制因素。

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