Summary
In cats lightly anesthetized with chloralose-urethane, vagal and carotid nerves dissected, the ventral surface of the medulla oblongata was perfused with mock CSF solutions. The pH of the fluids was varied by altering either the bicarbonate concentration or the CO2 pressure. During each period of perfusion steady stateP A CO2 response curves of respiration were recorded.
Tidal volume, respiratory frequency, and ventilation were plotted against a) the alveolar CO2 pressure, b) the pH of the perfusion fluids (pHCSF), and c) the pH in the extracellular space of the medulla (pHe). pHe was calculated from the acid base parameters of the blood and the mock CSF by means of a mathematical model described by Berndt, Berger and Mückenhoff (1972).
Under the conditions specified above respiration was neither a unique function ofP A CO2 nor of pHCSF. In a single experiment, severalP A CO2 response curves could be recorded, the number and position of which depended upon the number and the composition of the fluids simultaneously applied to the medullary surface. Similarly, pHCSF response curves could be constructed, the position and course of which was determined by theP A CO2.
On the other hand, respiration could be shown to be an almost unique function of the medullary extracellular pH—irrespective of whether pHe was changed by alteringP A CO2 or pHCSF—ifV T or were platted against the pHe values located at a depth of 200–400 μm below the ventral medullary surface. A worse correlation was obtained between respiration and pHe at smaller or greater depth.
It is concluded that the effects on respiration of changes in the CO2 pressure of the blood or in the bicarbonate concentration and the CO2 pressure of the CSF can be explained by their influence on the extracellular hydrogen ion concentration in the medulla. The chemosensitive structures responding to the hydrogen ion concentration have to be assumed at a location less than 1 mm below the ventral medullary surface.
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Berndt, J., Berger, W., Berger, K. et al. Untersuchungen zum zentralen chemosensiblen Mechanismus der Atmung. Pflugers Arch. 332, 146–170 (1972). https://doi.org/10.1007/BF00589090
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DOI: https://doi.org/10.1007/BF00589090