This is an application for supplemental funds to augment the statistical support required for our approved clinical and basic research on stroke and related problems in cerebral vascular disease and cerebral metabolism. The underlying program project consists of a clinical unit designed to evaluate early dynamic changes in stroke and to identify variables useful in gauging prognosis from stroke. The clinical studies are also directed at the quantification of edema in stroke and evaluation of its morbidity. Other clinical efforts are directed towards identifying neurochemical profiles in hypertensive stroke patients. Clinical neuropsychological studies will examine cognitive factors affecting recovery. Both clinical and basic studies are directed at platelet function in stroke. Fundamental laboratory studies examine cerebral energy metabolism and blood flow in evolving stroke, axoplasmic transport during anoxia-ischemia, and the effect of hypoxemia on acetylcholine metabolism in the brain. Examination of experimental stroke in the nonhuman primate will give an opportunity to examine the pathogenesis, metabolism, consequences, and potential treatment of focal ischemia in an animal model more closely resembling man. Experimental studies on blood brain barrier damage by anoxia-ischemia and the relation of such damage to cerebral edema are continuing. Other investigators in the project are examining the fundamental mechanisms and potential treatment of experimental neurogenic hypertension, in the role of changes in catecholamines in producing stroke and in the fundamental mechanisms of brain repair.
| Takeda, Yoshimasa; Zhao, Liang; Jacewicz, Michael et al. (2011) Metabolic and perfusion responses to recurrent peri-infarct depolarization during focal ischemia in the Spontaneously Hypertensive Rat: dominant contribution of sporadic CBF decrements to infarct expansion. J Cereb Blood Flow Metab 31:1863-73 |
| Petito, C K; Halaby, I A (1993) Relationship between ischemia and ischemic neuronal necrosis to astrocyte expression of glial fibrillary acidic protein. Int J Dev Neurosci 11:239-47 |
