Arteries with elastin deficiency demonstrate tortuosity in human and animals, but the underlying mechanism has not been clearly elucidated. Our previous studies suggested that mechanical instability is a mechanism that leads to vessel tortuosity [1]. The objective of this study was to determine the role of extracellular matrix proteins in maintaining the mechanical stability of arteries. To this end, two groups of porcine carotid arteries were treated with elastase (8U/ml) and collagenase (2000 U/ml) respectively and tested before and after the treatments. The arteries were tested for pressurized inflation and the data were fitted with a Fung strain energy function to determine their stress-strain relationship. The critical pressures, at which the arteries became unstable and started to bend, were determined by a buckling test. The specimens were then processed for elastin staining and collagen staining and microscopy examinations. Our results demonstrated that elastase and collagenase treatment led to significant decreases in wall stiffness and critical buckling pressure of arteries. For example, the pre- and post- elastase treatment critical pressures of arteries are 19.9±5.3 kPa and 9.1±3.6 kPa, respectively, at in vivo length (n=6. p<0.05, see Figure 1). These results suggested that elastin and collagen degradation reduced the stability of arteries making them more susceptible to buckling and that mechanical buckling could initiate vessel tortuosity.

Figure 1

Comparison of the critical pressure of arteries (mean±SD, n=6) measured before and after elastase treatment. ^* p < 0.05.