Skeletal muscle oxygen availability during respiratory acid-base disturbances in cats

Abstract

Respiratory acid-base disorders elicit physiological responses that alter O 2 delivery to various tissues. We have used a near infrared (NIR) optical technique to monitor cytochrome a, a 3 oxidation state, tissue O 2 store (relative hemoglobin plus myoglobin oxygenation), and regional blood volume in intact resting skeletal muscle during respiratory acid-base disturbances in anesthetized cats. Hypercapnic acidosis of hypercapnic alkalosis were produced in separate groups of animals by ventilation with increasing concentrations of CO 2 (n = 13) or hyperventilation (n = 8). Respiratory acidosis decreased oxygen availability to hindlimb muscle while respiratory alkalosis did not change tissue oxygenation. Inspired CO 2 progressively decreased muscle blood volume, cytochrome a, a 3 oxidation level, and muscle oxygen store. These optical responses were greatly attenuated both by pre-treatment with bretylium and by hemorrhagic hypotension, suggesting mediation through sympathetic vasoconstriction. Metabolic acidosis, produced by intravenous HCl infusion (n = 8), did not reproduce the hindlimb optical responses mediated by Co 2. These experiments demonstrate that hypercapnic acidosis significantly decreases oxygen supply to resting skeletal muscle in the anethetized cat, probably via neuroregulatory responses to CO 2 which do not depend on changes in arterial [H +] in tested pH range.