Cerebral resistance to anoxia in the marine turtle.

The extraordinary ability of the turtle to withstand prolonged anoxia was examined in cerebral cortex in situ by recording changes in the reduction/oxidation ratio of cytochrome a,a3 by reflection spectrophotometry. Inspiration of 100% oxygen increased the oxidation of cytochrome a,a3 beyond that of the air breathing control, suggesting that cytochrome a,a3 is not fully oxidized under normoxic conditions in turtle brain. A similar response was seen also in cerebral cortex of the rat. The significance of the cytochrome a,a3 reduction in these intact tissues is discussed. Both severe hypoxia (100% N2) and asphyxia produced increasing levels of reduced cytochrome a,a3 in turtle and rat brains. The rat of change produced by N2 inspiration was greater than that produced by asphyxia in both species. This is interpreted as demonstrating an open pulmonary blood circulation during anoxia. In turtles, levels of reduced cytochrome a,a3 were maintained for over 3 h of continual N2 inspiration. Subsequent inspiration of room air resulted in a full restoration of turtle brain cytochrome a,a3 redox state within 30 sex. In the rat, continued N2 inspiration resulted in a rapid reduction of cytochrome a,a3 to a plateau (3 min) which became irreversible within a short period. An extended tolerance of N2 inspiration found in rats cooled to temperatures approximating that of the turtle was inadequate to account for the wide species of difference. We suggest that special adaptations, not related to the redox state of cytochrome oxidase under normoxic conditions, are responsible for maintaining the functional integrity and the capacity for cytochrome oxidase re-oxidation of turtle brain mitochondria under prolonged anoxia.