Hyperoxia during reperfusion is a factor in reperfusion injury.

Imposition of ischemia should result in accumulation of lactic acid with an attendant drop in pH. Subsequent reperfusion would result in hyperoxia, in the affected tissue, due to the Bohr Effect. O2- should therefore be produced in greater than normal amounts, due to this transient hyperoxia, and may contribute to reperfusion injury. Tissue acidification, during extreme exercise or in diabetes mellitus, may similarly lead to hyperoxia and to tissue damage by O2-.