The overall hypothesis of this proposal is that traumatic brain injury (TBI) causes a reduction in CBF in the early post-injury period that contributes to the brain damage by 2-mechanisms: 1-if the reduction in CBF is severe enough and lasts long enough, ischemic injury (primary ischemia; occurs 2- if the reduction is CBF is more modest, ischemic injury may not occur, but the brain is more susceptible to secondary insults (secondary ischemia). Global reductions in CBF severe enough to result in ischemic injury (CBF,18 ml/100g/min) occur with very severe injuries and this finding is associated with a high mortality rate. Regional reductions in CBF severe enough to result in ischemic injury (rCBF<18 ml/100g/min) occur more commonly and are typically found in areas of brain contusion and underlying evacuated extracerebral hematomas. Even more commonly, a moderate reduction in CBF which is compensated by increased cerebral oxygen extraction occurs during the first few hours after TBI. This program projects will approach the problem of vascular changes after traumatic brain injury with both clinical and laboratory studies. There are 3 projects and 3 cores in the program project. Project 1. Regulation of Cerebral Blood Flow after Traumatic Brain Injury. Project 2. Increased Vascular Resistance after Traumatic Brain Injury. Project 3. L-arginine Treatment of a Reduced CBF after Traumatic Brain Injury. Core A. Administrative Core Core B. Statistical and Modeling Core Core C. Analytical Lab Core
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