Abstract

Cerebral function is lost within seconds of deprivation of oxygen and within 2–3 minutes anoxic depolarization begins (see Silver, 1977, 1978). This depolarization is characterized by massive loss of K+ and uptake of CI- into cells (Van Harrevald, 1971). If depolarizing conditions continue, there is progressive accumulation of intracellular Ca2+ and degradation of essential cellular components. The extent to which the loss of cellular and brain function can be reversed depends on the time and degree of oxygen deprivation as well as the conditions during and after reoxygenation. Attempts to define the biochemical and physiological parameters responsible for the irreversible damage have met with limited success (for review see Welsh et al, 1982; Raichle, 1983). Analytical limits in the quantitation of oxygen have been particularly vexing. Oxygen deprivation is a relative term and it is important to know the extent to which the residual flow and collateral circulation are providing oxygen to the tissue. Some measurements have been made by inserting small oxygen electrodes into the tissue (Silver, 1977; 1978; Nair et al, 1987; Fennema et al, 1989) or by multielectrode surface electrodes (Leniger-Follert, 1977; Grote et al, 1984). The former are limited to measuring at single points in the tissue and cause significant mechanical disruption of the tissue during insertion.

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