Respiratory function was evaluated in brain mitochondria prepared from rats subjected to either complete compression ischemia or pronounced incomplete hypotensive ischemia of 30 min duration, and from animals allowed a 30 min recirculation period following 30 min of ischemia. Oxygen utilization rates in the mitochondrial preparations were measured with an oxygen electrode in a closed and stirred chamber with glutamate plus malate or with succinate as substrates.
After 30 min of ischemia there was a decrease in respiratory control ratio (RCR), in state 3 respiratory activity and maximal phosphorylation rate whether ischemia was complete or incomplete. After recirculation following complete ischemia, mitochondria showed extensive functional recovery with normalization of RCR, as well as of state 3 and maximal phosphorylation rates. Following incomplete ischemia, there was a suggestive further deterioration of mitochondrial function. Addition of Mg++ did not reverse the pattern of respiratory inhibition. The results are in agreement with previous communications from this laboratory, demonstrating a nearly complete recovery of cerebral energy state upon recirculation after an equivalent period of complete compression ischemia but not after pronounced, incomplete hypotensive ischemia. The persistence of mitochondrial dysfunction during recirculation after incomplete ischemia indicates that a mitochondrial damage could be a primary factor for the deficient recovery of the cerebral energy state. Events during the initial recirculation period may be at least partly responsible for failure of energy metabolism.