Role of acid-base balance in the chemoreflex control of breathing
Author(s) -
James Duffin
Publication year - 2005
Publication title -
journal of applied physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.253
H-Index - 229
eISSN - 8750-7587
pISSN - 1522-1601
DOI - 10.1152/japplphysiol.00640.2005
Subject(s) - chemoreceptor , control of respiration , ventilation (architecture) , acid–base homeostasis , hyperventilation , peripheral chemoreceptors , central chemoreceptors , respiratory alkalosis , respiratory system , chemistry , anesthesia , respiration , medicine , biochemistry , metabolic acidosis , anatomy , receptor , thermodynamics , physics
This paper uses a steady-state modeling approach to describe the effects of changes in acid-base balance on the chemoreflex control of breathing. First, a mathematical model is presented, which describes the control of breathing by the respiratory chemoreflexes; equations express the dependence of pulmonary ventilation on Pco(2) and Po(2) at the central and peripheral chemoreceptors. These equations, with Pco(2) values as inputs to the chemoreceptors, are transformed to equations with hydrogen ion concentrations [H(+)] in brain interstitial fluid and arterial blood as inputs, using the Stewart approach to acid-base balance. Examples illustrate the use of the model to explain the regulation of breathing during acid-base disturbances. They include diet-induced changes in sodium and chloride, altitude acclimatization, and respiratory disturbances of acid-base balance due to chronic hyperventilation and carbon dioxide retention. The examples demonstrate that the relationship between Pco(2) and [H(+)] should not be neglected when modeling the chemoreflex control of breathing. Because pulmonary ventilation controls Pco(2) rather than the actual stimulus to the chemoreceptors, [H(+)], changes in their relationship will alter the ventilatory recruitment threshold Pco(2), and thereby the steady-state resting ventilation and Pco(2).
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