The efforts detailed within are steps in the overall goal of utilizing intracellular indicators of oxidative metabolic activity to assess the changes that occur during cerebral anoxia/ischemia and to determine the factors most critical to overall tissue viability during and following periods of circulatory compromise. Non-invasive techniques of fluorometrically monitoring changes in the reduction/oxidation ration of intramitochondrial NAD and the technique of reflection spectrophotometry to measure redox changes of cytochromes together with changes in hemoglobin oxygenation and local blood volume will be utilized. By relating parameters of metabolism and function, we will discern how vulnerability of functional activity is associated with periods of ischemic insult. We will continue efforts to define the relationships between energy metabolism and the functioning of the central nervous system to increase our understanding of how and why the brain uses oxygen, metabolic substrates and oxidative energy and to determine how viability is threatened by the loss of oxygen and circulatory perfusion.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Project (R01)
Project #
5R01NS014325-10
Application #
3395477
Study Section
Neurology A Study Section (NEUA)
Project Start
1977-08-01
Project End
1989-11-30
Budget Start
1987-12-01
Budget End
1988-11-30
Support Year
10
Fiscal Year
1988
Total Cost
Indirect Cost
Name
University of Miami School of Medicine
Department
Type
Schools of Medicine
DUNS #
City
Miami
State
FL
Country
United States
Zip Code
33101
Perez-Pinzon, M A; Born, J G (1999) Rapid preconditioning neuroprotection following anoxia in hippocampal slices: role of the K+ ATP channel and protein kinase C. Neuroscience 89:453-9
Centeno, J M; Orti, M; Salom, J B et al. (1999) Nitric oxide is involved in anoxic preconditioning neuroprotection in rat hippocampal slices. Brain Res 836:62-9
Sick, T J; Xu, G; Perez-Pinzon, M A (1999) Mild hypothermia improves recovery of cortical extracellular potassium ion activity and excitability after middle cerebral artery occlusion in the rat. Stroke 30:2416-21;discussion 2422
Sick, T J; Tang, R; Perez-Pinzon, M A (1999) Cerebral blood flow does not mediate the effect of brain temperature on recovery of extracellular potassium ion activity after transient focal ischemia in the rat. Brain Res 821:400-6
Perez-Pinzon, M A; Xu, G P; Born, J et al. (1999) Cytochrome C is released from mitochondria into the cytosol after cerebral anoxia or ischemia. J Cereb Blood Flow Metab 19:39-43
Perez-Pinzon, M A; Vitro, T M; Dietrich, W D et al. (1999) The effect of rapid preconditioning on the microglial, astrocytic and neuronal consequences of global cerebral ischemia. Acta Neuropathol (Berl) 97:495-501
Feng, Z C; Sick, T J; Rosenthal, M (1998) Oxygen sensitivity of mitochondrial redox status and evoked potential recovery early during reperfusion in post-ischemic rat brain. Resuscitation 37:33-41
Perez-Pinzon, M A; Mumford, P L; Carranza, V et al. (1998) Calcium influx from the extracellular space promotes NADH hyperoxidation and electrical dysfunction after anoxia in hippocampal slices. J Cereb Blood Flow Metab 18:215-21
Sick, T J; Feng, Z C; Rosenthal, M (1998) Spatial stability of extracellular potassium ion and blood flow distribution in rat cerebral cortex after permanent middle cerebral artery occlusion. J Cereb Blood Flow Metab 18:1114-20
Perez-Pinzon, M A; Mumford, P L; Sick, T J (1998) Prolonged anoxic depolarization exacerbates NADH hyperoxidation and promotes poor electrical recovery after anoxia in hippocampal slices. Brain Res 786:165-70

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