INHIBITION OF EPINEPHRINE ACTION IN SEVERE HYPOXEMIA

Abstract

Acute severe hypoxemia produced by N2 breathing in the anesthetized dog caused a gradual rise in arterial pressure, reaching a maximal level in 60-90 sec. Continuance of N2 breathing beyond this time is followed by a rapidly progressive fall in pressure to shock levels. Re-oxygenation after a period of falling blood pressure results in a marked rise in pressure. This post-hypoxemic pressor effect is attributed to the accumulation of pressor materials which do not act in the absence of O2. Epinephrine injn. during the hypoxe-mic depressor phase acts similarly in that its pressor action is held in abeyance until the animal is re-oxygenated. Some physiol. and clinical aspects of these findings are discussed.