Effect of oxygen on potassium-excited ventilation in the decerebrate cat

Abstract

Raising arterial potassium ([K +] a) from ca. 3.5 to 6.5mM, as occurs in heavy exercise, excites the arterial chemoreceptors and ventilation (V̇ e) in anaesthetised cats. We have previously shown that the excitation of chemoreceptors by potassium is enhanced by hypoxia and abolished by hyperoxia, and here we show, in decerebrate cats, that the potassium-induced increase in V̇ e is also abolished by hyperoxia. 100% oxygen was given abruptly in hypoxia ( Pet O2 ca. 50 Torr), with inspired gas tension sadjusted to give the same Pet O2 and Pet CO2 values before all tests on a given animal. Intravenous infusions of 150 mM KCl, which raised [K +] a from 3.9 ± 0.3 mM to 7.4 ± 0.3 mM (mean ± SE), always excited hypoxic V̇ e ( 42 ± 8%); P < 0.01. Hyperoxia, given during KCl infusion, reduced V̇ e to a value not significantly greater ( P > 0.27) than the hyperoxic value obtained before infusion. These results show that: (i) V̇ e reflects the responses of chemoreceptors to K +, (ii) that abrupt hyperoxia removes the potassium-induced ventilatory drive, and (iii) that, in our experiments, K + appears to have excited V̇ e only via the peripheral chemoreceptors.