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Dual contribution theory of regulation of CSF HCO3 in respiratory acidosis

Dual contribution theory of regulation of CSF HCO3 in respiratory acidosis of regulation acidosis of H. KAZEMI Medical Services (Pulmonary Unit), Massachusetts General Hospital Department of Medicine, Harvard Medical School, Boston, Massachusetts 02114 C02, catalyzed by the locally present carbonic anhydrase (32). When carbonic anhydrase (CA), found in abundance in the cells of choroid plexus in glia cells (9), was inhibited by injection of acetazolamide into the lateral cerebral ventricles, the expected rise in in respiratory acidosis was significantly impaired. Under these experimental conditions the increase in matched the increase in arterial plasma no enhanced in vivo buffering was apparent (32)+ These findings suggested the presence of two sources for the rise in respiratory acidosis (dual contribution theory): one locally formed within the. CNS catalyzed by carbonic anhydrase the other derived from plasma, probably by simple diffusion. The present investigation on regulation in respiratory acidosis was undertaken to quantitate the relationship between locally formed in the CNS from that derived from plasma by selectively varying plasma concentration in the absence or presence of inhibition of carbonic anhydrase in the central nervous system. The results demonstrate that in regulation of HCO,- in respiratory acidosis there is an interplay between the locally formed the increased plasma . The mechanism is such http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Applied Physiology The American Physiological Society

Dual contribution theory of regulation of CSF HCO3 in respiratory acidosis

Journal of Applied Physiology , Volume 40: 559 – Apr 1, 1976

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Publisher
The American Physiological Society
Copyright
Copyright © 1976 the American Physiological Society
ISSN
8750-7587
eISSN
1522-1601
Publisher site
See Article on Publisher Site

Abstract

of regulation acidosis of H. KAZEMI Medical Services (Pulmonary Unit), Massachusetts General Hospital Department of Medicine, Harvard Medical School, Boston, Massachusetts 02114 C02, catalyzed by the locally present carbonic anhydrase (32). When carbonic anhydrase (CA), found in abundance in the cells of choroid plexus in glia cells (9), was inhibited by injection of acetazolamide into the lateral cerebral ventricles, the expected rise in in respiratory acidosis was significantly impaired. Under these experimental conditions the increase in matched the increase in arterial plasma no enhanced in vivo buffering was apparent (32)+ These findings suggested the presence of two sources for the rise in respiratory acidosis (dual contribution theory): one locally formed within the. CNS catalyzed by carbonic anhydrase the other derived from plasma, probably by simple diffusion. The present investigation on regulation in respiratory acidosis was undertaken to quantitate the relationship between locally formed in the CNS from that derived from plasma by selectively varying plasma concentration in the absence or presence of inhibition of carbonic anhydrase in the central nervous system. The results demonstrate that in regulation of HCO,- in respiratory acidosis there is an interplay between the locally formed the increased plasma . The mechanism is such

Journal

Journal of Applied PhysiologyThe American Physiological Society

Published: Apr 1, 1976

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