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Research Article Free access | 10.1172/JCI105538
Department of Medicine, Tufts University School of Medicine, and the Renal Laboratory, New England Medical Center Hospitals, Boston, Mass.
†Work done during tenure of a postdoctoral research fellowship of the U. S. Public Health Service.
‡Address requests for reprints to Dr. William B. Schwartz, New England Medical Center Hospitals, 171 Harrison Ave., Boston, Mass. 02111.
*Submitted for publication July 5, 1966; accepted November 10, 1966.
Supported in part by grants H-759 and HE 5309 from the National Heart Institute and by a grant from the American Heart Association.
Find articles by Sapir, D. in: JCI | PubMed | Google Scholar
Department of Medicine, Tufts University School of Medicine, and the Renal Laboratory, New England Medical Center Hospitals, Boston, Mass.
†Work done during tenure of a postdoctoral research fellowship of the U. S. Public Health Service.
‡Address requests for reprints to Dr. William B. Schwartz, New England Medical Center Hospitals, 171 Harrison Ave., Boston, Mass. 02111.
*Submitted for publication July 5, 1966; accepted November 10, 1966.
Supported in part by grants H-759 and HE 5309 from the National Heart Institute and by a grant from the American Heart Association.
Find articles by Levine, D. in: JCI | PubMed | Google Scholar
Department of Medicine, Tufts University School of Medicine, and the Renal Laboratory, New England Medical Center Hospitals, Boston, Mass.
†Work done during tenure of a postdoctoral research fellowship of the U. S. Public Health Service.
‡Address requests for reprints to Dr. William B. Schwartz, New England Medical Center Hospitals, 171 Harrison Ave., Boston, Mass. 02111.
*Submitted for publication July 5, 1966; accepted November 10, 1966.
Supported in part by grants H-759 and HE 5309 from the National Heart Institute and by a grant from the American Heart Association.
Find articles by Schwartz, W. in: JCI | PubMed | Google Scholar
Published March 1, 1967 - More info
We have carried out balance studies in normal dogs in order to appraise the effects of chronic hypoxemia on acid—base and electrolyte equilibrium. During the first phase of observation we produced a state of “pure” hypoxemia by reducing the oxygen concentration (utilizing nitrogen as a diluent) and by adding carbon dioxide to the environment in a concentration sufficient to keep arterial CO2 tension (PCO2) within normal limits. The data demonstrate that such a 9-day period of normocapneic hypoxemia has no effect on electrolyte excretion and is virtually without effect on plasma composition.
During the second phase of observation we subjected the hypoxemic dogs to stepwise increments in arterial carbon dioxide tension in order to evaluate the effects of the low oxygen tension on the acid—base adjustments to a chronic state of hypercapnia. At least 6 days was allowed for extracellular composition to reach a new steady state at each level of inspired carbon dioxide. The data demonstrate a rise in both plasma bicarbonate concentration and renal acid excretion that was not significantly different from that which has been described previously for hypercapnia without hypoxemia. Just as in these earlier studies, plasma hydrogen ion concentration rose with each increment in carbon dioxide tension, each millimeter Hg increment in PCO2 leading to an increase in hydrogen ion concentration of 0.32 nmole per L. It thus appears that the chronic“carbon dioxide response curve” is not significantly influenced by moderately severe hypoxemia.