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J Appl Physiol 63: 2084-2092, 1987;
8750-7587/87 $5.00
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Journal of Applied Physiology, Vol 63, Issue 5 2084-2092, Copyright © 1987 by American Physiological Society


ARTICLES

Differential effects of oligomycin on carotid chemoreceptor responses to O2 and CO2 in the cat

M. Shirahata, S. Andronikou and S. Lahiri
Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia 19104-6085.

Effects of oligomycin on carotid chemoreceptor responses to O2 and CO2 were investigated using an in situ perfusion technique. Cats were anesthetized, paralyzed, and artificially ventilated. To avoid a possible reaction between an oligomycin-ethanol mixture and blood, we administered oligomycin to the carotid body via cell- and protein-free perfusate. Except for the perfusion periods, the carotid body received its own natural blood supply. Responses to O2, CO2, sodium cyanide, and nicotine of the same carotid chemoreceptor afferents were studied before and after each perfusion. An appropriate low dose of oligomycin completely blocked carotid chemoreceptor response to O2 while preserving the CO2 response. At the same time cyanide response was attenuated leaving nicotine response intact. Additional doses of oligomycin attenuated carotid chemoreceptor response to CO2 as well. Perfusion with a blank solution containing ethanol did not change the carotid body chemoreceptor responses. These effects of oligomycin on carotid chemoreceptor responses to O2 and CO2 were reversible, and restoration of the response to CO2 preceded that to O2. In addition, oligomycin administered into the blood with close intra-arterial injection produced similar differential blockade of O2 and CO2 chemoreception, preserving the nicotine and dopamine effects. This study confirmed the previous findings and provided new evidence showing that 1) the responses of carotid chemoreceptor to O2 and CO2 were separable by oligomycin due to the inhibition of oxidative phosphorylation and 2) the responses to nicotine and dopamine were intact even after blockade of O2 response.





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