Date of Award

1995

Degree Type

Dissertation

Degree Name

Doctor of Philosophy

Abstract

The respiratory system regulates alveolar ventilation (V{dollar}\sb{lcub}\rm A{rcub}{dollar}) almost exactly to the demands of the body so that the PCO{dollar}\sb2{dollar} and PO{dollar}\sb2{dollar} of the arterial blood are hardly altered, even during strenuous exercise or other types of respiratory stress. The feedback control of ventilation was studied in human subjects using the technique of dynamic end-tidal forcings to produce perturbations in end-tidal PCO{dollar}\sb2{dollar} (P{dollar}\sb{lcub}\rm ET{rcub}{dollar}CO{dollar}\sb2{dollar}) and end-tidal PO{dollar}\sb2{dollar} (P{dollar}\sb{lcub}\rm ET{rcub}{dollar}O{dollar}\sb2{dollar}) to stimulate the respiratory chemoreceptors.;The purpose of the first study was to investigate the interaction between ventilatory drives from the central (cR{dollar}\sb{lcub}\rm c{rcub}{dollar}) and peripheral (pR{dollar}\sb{lcub}\rm c{rcub}{dollar}) chemoreceptors using their different speeds of response to enable a temporal separation of their chemical stimulation. It was demonstrated that the chemoreflexes were independent of each other, confirming that hypoxia and the CO{dollar}\sb2{dollar}-H{dollar}\sp+{dollar} complex interact at the level of the pR{dollar}\sb{lcub}\rm c{rcub}{dollar}, and the drives from the periphery and from the central chemosensitive area add together in their effects on ventilation.;The objective of the second study was to examine the contribution of the pR{dollar}\sb{lcub}\rm c{rcub}{dollar} to ventilation during the steady state of moderate intensity exercise, using hyperoxic suppression of pR{dollar}\sb{lcub}\rm c{rcub}{dollar} drive, while stabilizing the drive at the cR{dollar}\sb{lcub}\rm c{rcub}{dollar} by maintaining a constant P{dollar}\sb{lcub}\rm ET{rcub}{dollar}CO{dollar}\sb2{dollar}. The results revealed that the peripheral chemoreceptors were responsible for 15% of the ventilatory drive during moderate intensity exercise. This modest contribution supports the theory that the arterial chemoreceptors function to "fine tune" V{dollar}\sb{lcub}\rm A{rcub}{dollar} to minimize change in arterial blood gases. Sustained hyperoxia, however, appeared to lower the set point about which P{dollar}\sb{lcub}\rm a{rcub}{dollar}CO{dollar}\sb2{dollar} was regulated.;The technique of dynamic end-tidal forcings is based on the assumption that changes in P{dollar}\sb{lcub}\rm ET{rcub}{dollar}CO{dollar}\sb2{dollar} mirror changes in P{dollar}\sb{lcub}\rm a{rcub}{dollar}CO{dollar}\sb2{dollar}. The objective of the final study was to compare arterial PCO{dollar}\sb2{dollar} (P{dollar}\sb{lcub}\rm a{rcub}{dollar}CO{dollar}\sb2{dollar}), determined directly in the radial artery, with indirect estimates of P{dollar}\sb{lcub}\rm a{rcub}{dollar}CO{dollar}\sb2{dollar} derived from arterialized-venous blood (P{dollar}\sb{lcub}\rm av{rcub}{dollar}CO{dollar}\sb2{dollar}) and from the respired gases. Mean (P{dollar}\sb{lcub}\rm av{rcub}{dollar}CO{dollar}\sb2{dollar}) agreed most closely with mean P{dollar}\sb{lcub}\rm a{rcub}{dollar}CO{dollar}\sb2{dollar} at rest and in exercise. A significant P{dollar}\sb{lcub}\rm ET{rcub}{dollar}CO{dollar}\sb2{dollar} to P{dollar}\sb{lcub}\rm a{rcub}{dollar}CO{dollar}\sb2{dollar} difference, positively correlated with the level of inspired PCO{dollar}\sb2{dollar}, was found under both resting and exercise conditions. Of the noninvasive techniques, mean estimates calculated using the regression equation developed by Jones et al. (J. Appl. Physiol., 1979) corresponded most closely with P{dollar}\sb{lcub}\rm a{rcub}{dollar}CO{dollar}\sb2{dollar} in exercise.

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