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December 1973

Brain Mitochondrial Function After Ischemia and Hypoxia: II. Normotensive Systemic Hypoxemia

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;

Arch Neurol. 1973;29(6):417-419. doi:10.1001/archneur.1973.00490300079010

Respiratory function of rabbit brain mitochondria was well maintained after 37 minutes of severe systemic, normotensive hypoxemia. Respiratory control ratios and some state 3 rates were above normal, suggesting "tighter" coupling and lack of respiratory inhibition at cerebral venous oxygen tensions as low as 8 mm Hg and arterial oxygen tensions as low as 11 mm Hg. These findings agree with those of MacMillan and Siesjo, who found no change in the energy charge or nicotinamide adenine nucleotide dehydrogenase: nicotinamide adenine dinucleotide ratio after profound hypoxemia. Conventional concepts of brain tissue oxygenation are challenged by these findings. In addition, evidence supports the experiments of Eklof and Siesjo which show that cerebral venous oxygen tensions are inaccurate in defining tissue oxygenation at low perfusion pressures. Brain mitochondria were "loosely" coupled and inhibited under hypotensive and hypoxemic conditions.

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