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Brain Mitochondrial Function After Ischemia and HypoxiaII. Normotensive Systemic Hypoxemia
Hart Schutz, MD;
Peter R. Silverstein, MD;
Matti Vapalahti, MD;
Derek A. Bruce, MD;
Lena Mela, MD;
Thomas W. Langfitt, MD
Arch Neurol. 1973;29(6):417-419.
Abstract
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.
Author Affiliations
Philadelphia
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;
Footnotes
Accepted for publication July 3, 1973. and Dr. Vapalahti is with the Neurosurgery Division, University of Turku, Turku, Finland.
Reprint requests to Division of Neurosurgery, Hospital of the University of Pennsylvania, 3400 Spruce St, Philadelphia 19104 (Dr. Langfitt).
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