Untitled Eckardt Thesis by A. Sidwell

Abstract Traumatic brain injury (TBI) is a leading cause of death and disability in persons under 35 years of age. In nonfatal moderate to severe TBI, secondary cellular edema causes long-lasting brain damage. Vasopressin mediates the expression of aquaporin 4 after injury, a protein that regulates water uptake into cells and thus contributes to brain swelling. I examined the role of vasopressin in aquaporin 4 upregulation in chemical and mechanical models of TBI. Vasopressin was used to simulate TBI conditions in culture and upregulated aquaporin 4 following injury condition. A blast device was created to simulate blast injury conditions in vitro. Future experiments are needed to refine device parameters and its potential use as a high throughput screening mechanism for drugs that can potentially treat TBI.