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Independence of Blood and Cerebrospinal Fluid Lactate
Jerome B. Posner, MD;
Fred Plum, MD
Arch Neurol. 1967;16(5):492-496.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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A RISE in lactic acid concentration in body fluids implies altered tissue metabolism which can take two forms. If pyruvic acid rises in proportion to the increase in lactic acid, both changes can be attributed to an increased breakdown of glucose or to a decreased entry of pyruvic acid into the Krebs metabolic cycle. Such alterations are produced by systemic alkalosis, glucose infusions, and epinephrine injections and are clinically benign.1 If, on the other hand, pyruvate fails to rise in proportion to the rise in lactate, "excess lactate" is produced.2 Production of excess lactate is believed to be due to anaerobic glycolysis and to represent clinically ominous tissue hypoxia.
Since the brain uses glucose as its only exogenous substrate and is totally dependent upon aerobic metabolism for its continued existence, cerebral metabolic abnormalities can be expected to rapidly alter lactic acid levels in the surrounding cerebral tissue fluids.
. . . [Full Text PDF of this Article]
Author Affiliations
New York
From the Department of Neurology, Cornell University Medical College, New York.
Footnotes
Submitted for publication Dec 19, 1966; accepted Jan 14, 1967.
Read in part before the American Academy of Neurology Meeting, Philadelphia, April 28-30.
Reprint requests to Department of Neurology, New York Hospital-Cornell Medical Center, 525 E 68th St, New York 10021 (Dr. Posner).
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