Journal of Applied Physiology Watch the video to learn how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Appl Physiol 53: 413-418, 1982;
8750-7587/82 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bidani, A.
Right arrow Articles by Crandall, E. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bidani, A.
Right arrow Articles by Crandall, E. D.

Journal of Applied Physiology, Vol 53, Issue 2 413-418, Copyright © 1982 by American Physiological Society


ARTICLES

Analysis of the effects of hematocrit on pulmonary CO2 transfer

A. Bidani and E. D. Crandall

A mathematical model of the chemical and transport events in blood during and after gas exchange has been used to examine the rates of CO2 excretion (Vco2) and O2 uptake (Vo2) in the lung at different levels of hematocrit (Hct), assuming fixed mixed venous blood O2 and CO2 contents and alveolar gases and constant cardiac output. The results show that a reduction in Hct from 45 to 30% leads to approximately 25% reduction in Vco2 compared with approximately 30% reduction in Vo2. Reduction of Hct from 45 to 15% results in approximately 50% reduction in Vco2 and approximately 63% reduction in Vo2. An increase in Hct from 45 to 60% results in approximately 25% increase in Vco2, accompanied by approximately 30% increase in Vo2. These fractional changes in gas exchange are only slightly affected by the extent of catalysis of the plasma CO2-H2CO3 hydration-dehydration reactions in the pulmonary vasculature. The reduction in Vco2 with reductions in Hct are due to 1) decrease in the total quantity of Bohr protons released during diminution of Vo2, 2) decrease in the size of the high buffer capacity intraerythrocytic pool, and 3) decrease in the total surface area available for HCO-3/Cl- exchange across the red cell membrane. We conclude that hitherto unrecognized changes in Vco2 (in addition to the well-known changes in Vo2) may occur as a consequence of alterations in Hct.


This article has been cited by other articles:


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
K. M. Gilmour and S. F. Perry
Branchial membrane-associated carbonic anhydrase activity maintains CO2 excretion in severely anemic dogfish
Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2004; 286(6): R1138 - R1148.
[Abstract] [Full Text] [PDF]


Home page
J. Exp. Biol.Home page
E. Stabenau and T. Heming
CO2 excretion and postcapillary pH equilibration in blood-perfused turtle lungs
J. Exp. Biol., January 4, 1999; 202(8): 965 - 975.
[Abstract] [PDF]


Home page
J. Appl. Physiol.Home page
V. Cardenas Jr., T. A. Heming, and A. Bidani
Kinetics of CO2 excretion and intravascular pH disequilibria during carbonic anhydrase inhibition
J Appl Physiol, February 1, 1998; 84(2): 683 - 694.
[Abstract] [Full Text] [PDF]


Home page
J. Appl. Physiol.Home page
S. Deem, M. K. Alberts, M. J. Bishop, A. Bidani, and E. R. Swenson
CO2 transport in normovolemic anemia: complete compensation and stability of blood CO2 tensions
J Appl Physiol, July 1, 1997; 83(1): 240 - 246.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online