Extracellular potassium homeostasis in the cat medulla during progressive brain hypoxia

Brain extracellular potassium ([K⁺](ec)) in the ventral respiratory group of the medulla and the phrenic neurogram were recorded in anesthetized vagotomized peripherally chemodenervated ventilated cats during progressive isocapnic carbon monoxide (CO) hypoxia. During hypoxia, the phrenic neurogram was progressively depressed and became silent when arterial O₂ content (Ca(O₂)) was reduced by 62 ± 3% (SE). Gasping was seen in the phrenic neurogram when Ca(O₂) was reduced by 78 ± 1%. Medullary [K⁺](ec), an indicator of energy production failure due to O₂ insufficiency, was 3.2 ± 0.4 mM before hypoxia and was statistically unchanged at the onset of phrenic apnea during CO hypoxia (4 ± 0.7 mM). By the onset of gasping, [K⁺](ec) had increased to 6.1 ± 1 mM, a value that tended to be different from control (P < 0.1). After initiation of gasping, the rate of rise of [K⁺](ec) increased, and [K⁺](ec) reached a maximum value of 14.3 ± 2.7 mM before hypoxia was terminated. With reoxygenation, [K⁺](ec) returned to control levels within 20 min. On the basis of these results, we have drawn two major conclusions. 1) Hypoxic depression to the point of phrenic apnea does not appear to be caused by medullary energy insufficiency as measured by loss of [K⁺](ec) homeostasis. 2) The rapid rise in [K⁺](ec) in the medulla that characterizes severe several hypoxia is closely associated with the onset of gasping in the phrenic neurogram, suggesting that gasping may serve as a marker for loss of medullary ionic homeostasis and thus onset of medullary energy insufficiency during hypoxia.