Collagen digestion mimics strain-induced softening in cerebral arteries.

Cerebral blood vessels are commonly injured in both trauma and surgical procedures. Constitutive damage models that predict vessel response to injury are critical to improved prevention and treatment. Prior research shows that stretch alters vessel mechanical properties but that denaturation of the collagen molecule only occurs at strains exceeding the yield point. The objective of this research was to clarify the role of collagen in sub-yield, stretch-induced softening of cerebral arteries. Two sets of experiments were conducted. In the first, native and collagen-digested sheep middle cerebral arteries (MCAs) were axially stretched to various magnitudes. Stretch-induced softening was compared between the two groups. In the second experiment, changes in MCA mechanical properties resulting from 60 min of continuous collagen digestion were characterized, and softening patterns were compared to those induced by overstretch in native vessels in the first experiment. In both experiments, collagen denaturation was evaluated using collagen hybridizing peptide (CHP). Results show that collagen digestion reduces the extent of softening caused by subsequent overstretch and that softening patterns resulting from collagen digestion mimic those caused by stretch. No consistent collagen denaturation was observed in overstretch experiments. These results together suggest that non-denaturing changes to collagen, and/or alteration of its connections to surrounding constituents, contribute substantially to sub-yield, overstretch-induced softening. Responsible mechanisms are yet to be defined.