| Despite decades of study, the precise mechanism by which the carotid body transduces the hypoxic stimulus remains controversial. CO inhibits carotid body output; Prabhakar has recently hypothesized that heme oxygenase 2 (HO-2) located in the glomus cells is the oxygen sensor, and that during hypoxia, endogenous CO production by HO-2 decreases, which disinhibits the carotid body. It was hypothesized that human subjects with mild carboxyhemoglobinemia would exhibit a reduced ventilatory response to hypoxia. Ten healthy male volunteers performed iso-oxic rebreathing tests at PO2 of 50 and 150 mmHg before and after inhalation of ∼1200 ppm CO in air, resulting in COHb values of 10.2 +/- 0.2% (mean +/- SEM). No statistically significant differences in threshold or sensitivity were observed due to CO. Mild increases in COHb in healthy humans do not affect chemoreflex sensitivity, suggesting that endogenous CO production may not be important in transducing the hypoxic stimulus. |
