Abstract
Earlier studies [1, 4] have shown that even a brief hypoxia leads to longlasting intracellular and extracellular lactacidosis in the brain. The CSF remains acidotic for prolonged periods even after a transient tissue hypoxia.
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Kaasik, A. E., L. Nilsson, and B. K. Siesjö: Acid-Base and Lactate/Pyruvate Changes in Brain and CSF in Asphyxia and Stagnant Hypoxia. Scand. J. din. Lab. Invest. Suppl. 102, p. III:C (1968).
Kaasik, A. E., L. Nilsson, and B. K. Siesjö: Reduction of Cerebral Arteriovenous Oxygen Difference in Terminal Phase of Cerebral Haemorrhage. Scand. J. din. Lab. Invest. Suppl. 102, p. X:D (1968).
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Zupping R., A. Tikk, and E. Kross: Some Biochemical Mechanisms of Brain Damage in Cases with Brain Injury, 1969, in press.
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© 1969 Springer-Verlag Berlin · Heidelberg
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Kaasik, A.E., Zupping, R. (1969). Correlations between Brain Gas Exchange and CSF Acid-Base Status in Patients with Cerebral Hemorrhage. In: Brock, M., Fieschi, C., Ingvar, D.H., Lassen, N.A., Schürmann, K. (eds) Cerebral Blood Flow. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-85860-4_42
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DOI: https://doi.org/10.1007/978-3-642-85860-4_42
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