Master of Science

thesisTraumatic brain injury (TBI) affects an estimated 1.7 million people annually in the United States, 52,000 of whom die as a result of TBI. TBI causes blood vessel dysfunction, and even in cases where hemorrhage is not present, TBI has been linked to long-term effects such as stroke. While vascular dysfunction is understood as a common outcome of TBI, the physiological and biochemical causes of dysfunction are not well understood. Better understanding of the nature of morphological damage to blood vessels will provide guidance in the development of therapies to treat TBI. This study investigates the effectiveness of collagen mimetic peptide (CMP) as a marker for mechanical damage to cerebral blood vessels exposed to various levels of axial overstretch. Eleven middle cerebral artery (MCA) segments from three lambs were exposed to four levels of axial overstretch. Seventeen sets of confocal images were recorded, with at least one set of images from each vessel. These images were analyzed for four different metrics in an attempt to quantify the difference between control and damaged samples. Examination of the images showed a number of bright streaks in the adventitia of the damaged samples. It is postulated that these streaks correspond to fibrous, axially oriented collagen structures in the adventitia of the blood vessels. Quantification of the percent of each image above a threshold value showed a significant difference between control samples, and those pulled to failure (p = .0032). This metric was shown to generally increase with increasing local stretch levels. This study shows that CMP is an effective marker for collagen damage due to axial overstretch