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Regulation of CSFHCO3- during long-term hypoxic hypocapnia in man

Regulation of CSFHCO3- during long-term hypoxic hypocapnia in man long-term hypoxic H. V. FORSTER, L. W. CHOSY, P. G. HANSON, AND (With the Technical Assistance of M. A. Sab and J. M. Vaughn) Pulmonary Physiology Laboratory, Department of Preventive Medice, University of Wiscons Medical School, Madison, Wiscons 53706 W. G. REDDAN [HCO,-] and a “-specific” or local via mechanisms that are dependent of changes plasma [HCO,--1. It has been commonly held that -specific mechanisms domate [ HCO,-] because of the relatively close protection afforded pH mabolic acidosis and alkalosis (8, 16). However, primary respiratory acid-base disturbances two types of evidence have accumulated which implicate an important role for changes systemic bicarbonate as a key nonspecific regulator of [HC03-1. First, respiratory acidosis (1, 2) or respiratory alkalosis the sojourner to high altitude (3, 5, 6, 10, ZZ), compensation of [H+] was shown to be comple and equal to that observed plasma. More recently, we and others have shown short-term hypocapnia or hypoxic hypocapnia anesthized dogs that most or all of the compensatory reduction [HCO,-] was prevented when arterial (or cerebral venous) plasma [HCO,-] was held constant via NaHCO, fusion (4, 24, 25). The present study has extended the design of these latter studies to man and to conditions http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Applied Physiology The American Physiological Society

Regulation of CSFHCO3- during long-term hypoxic hypocapnia in man

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Publisher
The American Physiological Society
Copyright
Copyright © 1978 the American Physiological Society
ISSN
8750-7587
eISSN
1522-1601
Publisher site
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Abstract

long-term hypoxic H. V. FORSTER, L. W. CHOSY, P. G. HANSON, AND (With the Technical Assistance of M. A. Sab and J. M. Vaughn) Pulmonary Physiology Laboratory, Department of Preventive Medice, University of Wiscons Medical School, Madison, Wiscons 53706 W. G. REDDAN [HCO,-] and a “-specific” or local via mechanisms that are dependent of changes plasma [HCO,--1. It has been commonly held that -specific mechanisms domate [ HCO,-] because of the relatively close protection afforded pH mabolic acidosis and alkalosis (8, 16). However, primary respiratory acid-base disturbances two types of evidence have accumulated which implicate an important role for changes systemic bicarbonate as a key nonspecific regulator of [HC03-1. First, respiratory acidosis (1, 2) or respiratory alkalosis the sojourner to high altitude (3, 5, 6, 10, ZZ), compensation of [H+] was shown to be comple and equal to that observed plasma. More recently, we and others have shown short-term hypocapnia or hypoxic hypocapnia anesthized dogs that most or all of the compensatory reduction [HCO,-] was prevented when arterial (or cerebral venous) plasma [HCO,-] was held constant via NaHCO, fusion (4, 24, 25). The present study has extended the design of these latter studies to man and to conditions

Journal

Journal of Applied Physiology – The American Physiological Society

Published: Feb 1, 1978

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