Elsevier

Brain Research

Volume 684, Issue 2, 3 July 1995, Pages 194-200
Brain Research

Reciprocal photolabile O2 consumption and chemoreceptor excitation by carbon monoxide in the cat carotid body: evidence for cytochrome a3 as the primary O2 sensor

https://doi.org/10.1016/0006-8993(95)00420-UGet rights and content
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Abstract

High carbon monoxide (CO) gas tensions (> 500 Torr) at normoxic PO2 (125–140 Torr) stimulates carotid chemosensory discharge in the perfused carotid body (CB) in the absence but not in the presence of light. According to a metabolic hypothesis of O2 chemoreception, the increased chemosensory discharge should correspond to a photoreversible decrease of O2 consumption, unlike a non-respiratory hypothesis. We tested the respiratory vs. non-respiratory hypotheses of O2 chemoreception in the cat CB by measuring the effect of high CO. Experiments were conducted using CBs perfused and superfused in vitro with high CO in normoxic, normocapnic cell-free CO2double bondHCO3 buffer solution at 37° C. Simultaneous measurements of the rate of O2 disapperance with recessed PO2 microelectrodes and chemosensory discharge were made after flow interruption with and without CO in the perfusate. The control O2 disappearance rate without CO was −3.66 ± 0.43 (S.E.) Torr/s (100 measurements in 12 cat CBs). In the dark, high CO reduced the O2 disappearance rate to −2.35 ± 0.33 Torr/s, or 64.2 ± 9.0% of control (P < 0.005, 34 measurements). High CO was excitatory in the dark, with an increase in baseline neural discharge from 129.2 ± 47.0 to 399.3 ± 49.1 impulses per s (P < 0.0001), and maximum discharge rate of 659 ± 76 impulses/s (N.S. compared to control) during flow interruption. During perfusion with high CO in the light, there were no significant differences in baseline neural discharge or in the maximum neural discharge after flow interruption, and little effect on O2 metabolism (88.8 ± 11.5% of control, N.S., 29 measurements). Thus the photoreversible decrease of O2 consumption and chemosensory excitation in the CO-treated CB is consistent with the metabolic theory of O2 chemoreception.

Keywords

Carbon monoxide
Carotid body
Chemoreceptor excitation
Cytochrome a32+
O2 consumption
PO2 microelectrode

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