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December 1973

Brain Mitochondrial Function After Ischemia and Hypoxia: I. Ischemia Induced by Increased Intracranial Pressure

Author Affiliations

From the Department of Surgery and Division of Neurosurgery, University of Pennsylvania, Philadelphia. Dr. Schutz is now with the Division of Neurosurgery, Toronto Western Hospital; Dr. Silverstein is at Hartford (Conn) Hospital; and Dr. Vapalahti is with the Neurosurgery Division, University of Turku, Turku, Finland.

Arch Neurol. 1973;29(6):408-416. doi:10.1001/archneur.1973.00490300070009

The effect of "compression ischemia" on brain mitochondrial activity was examined in 61 rabbits. We found that (1) the respiratory control ratio was significantly decreased only after 30 and 40 minutes of compression ischemia due to a decrease in state 3 and an increase in state 4 respiration; (2) heavy uncoupling of respiration occurred only after 40 minutes of compression ischemia; (3) uncoupler-activated adenosine triphosphatase (ATPase) was not impaired even after 40 minutes of ischemia, but spontaneous ATPase activity increased significantly; (4) secondary deterioration of mitochondrial function after circulatory recovery did not occur even with severe hypercapnia and hypocapnia in the recovery period as long as the cerebral perfusion pressure was maintained.

The findings suggest that alterations in constituents of the cell other than the mitochondria are responsible for irreversible brain damage following brief periods of total cerebral ischemia.

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