The biomechanical response of tissues serves as a valuable marker in the prediction of disease and in understanding the related behavior of the body under various disease and age states. Alterations in the macroscopic biomechanical response of diseased tissues are well documented; however, a thorough understanding of the microstructural events that lead to these changes is poorly understood. In this article we introduce a novel microbiaxial optomechanical device that allows two-photon imaging techniques to be coupled with macromechanical stimulation in hydrated planar tissue specimens. This allows that the mechanical response of the microstructure can be quantified and related to the macroscopic response of the same tissue sample. This occurs without the need to fix tissue in strain states that could introduce a change in the microstructural configuration. We demonstrate the passive realignment of fibrous proteins under various types of loading, which demonstrates the ability of tissue microstructure to reinforce itself in periods of high stress. In addition, the collagen and elastin response of tissue during viscoelastic behavior is reported showing interstitial fluid movement and fiber realignment potentially responsible for the temporal behavior. We also demonstrate that nonhomogeneities in fiber strain exist over biaxial regions of assumed homogeneity.

The modeling of drug delivery into tissues utilizes coupled convective and diffusive transport and therefore requires the experimental determination of the governing constants used in these models [1, 2]. The use of minimally destructive methods to determine these properties ensures increased accuracy [3]. Having the ability to test for strain or intraluminal pressure dependence also provides improved accuracy to the definitions of these properties.

The use of transgenic mice is an incredibly powerful tool in understanding the underlying etiology of disease. To understand the usefulness of specific transgenic mice, the systems of interest should be characterized. We have created TGFβ2-deficient mouse fetuses that develop widespread aortic and coronary artery aneurysms [1]. Several studies have pointed to a strong connection between elevated TGFβ signaling and aortic aneurysm [2]. In situ hybridization has shown that Tgfb2 and Tgfb3 are major ligands expressed in the aortic medial wall. Further reduction of TGFβ signaling by combining TGFβ2- and TGFβ3-deficient mice exacerbated cardiovascular aneurysms in TGFβ2/TGFβ3-doubly deficient embryos. In vitro cell culture experiments demonstrated an impaired ability of TGFβ2-deficient mouse embryonic fibroblasts to reorganize collagen. Previous data indicate reduced levels of TGFβ2 leading to a higher susceptibility to aortic aneurysm. We present here the macroscopic biomechanical characterization of the aorta of a transgenic mouse line showing this susceptibility and compare it to wild-type mice. We also present results comparing the microstructure between mouse lines.

It has been shown that the mechanical properties of tissue change significantly with age and under different disease states [1]. Specifically, blood vessels have shown that modified mechanical properties can be a predictor of impending disease such as advanced atherosclerosis or aneurysm [2].