Regional brain PO2 after global ischemia in monkeys: evidence for regional differences in critical perfusion pressures

Nemoto, E.M.; Erdmann, W.; Strong, E.; Rao, G.R.; Moossy, J.

Stroke 10(1): 44-52

1979


ISSN/ISBN: 0039-2499
PMID: 107623
DOI: 10.1161/01.str.10.1.44
Accession: 068520862

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Abstract
Brain tissue PO2 in the frontal and occipital cortices, mid-brain and basal ganglia were measured in monkeys [Macaca mulatta] for up to 5 h after 16 min global brain ischemia study those factors responsible for the selective vulnerability of the brain to ischemic anoxia. Brain tissue PO2 measurements were made with Au microelectrodes with tip diameters of 5-10 .mu.m. Reoxygenation of the different brain regions occurred at different apparent cerebral perfusion pressures and postischemia. Areas of low susceptibility to ischemic brain damage, such as the frontal cortex, were not consistently reoxygenated at lower perfusion pressures or earlier postischemia as were areas of high susceptibility such as the occipital cortex basal ganglia and midbrain. Earlier observations that perfusion defects and brain histologic changes are multifocal in nature after global brain ischemia were supported. Selective vulnerability of the brain to ischemia may be attributable to the development of regional edema and local increase in tissue pressure during ischemia which decreases cerebral perfusion pressure and leads to local perfusion defects after restoration of circulation. The selective vulnerability of the brain is attributable to variable degrees of neuronal-glial edema and regional shifts in brain H20 during ischemia leading to development of local perfusion defects and expansion of lesions from areas of high to low vulnerability.