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To investigate the mechanisms which enable the diaphragm to preserve ventilation when the work of breathing is elevated, we measured diaphragmatic blood flow (Q di) and oxygen consumption (VO2 di) in lightly anesthetized dogs. The animals were studied when they breathed quietly, when they inhaled 5% CO2 in 21% or 14% O2, or when they inhaled these gas mixtures through moderate to severe inspiratory resistances. Q di was determined from the integrated diaphragmatic arteriovenous difference of krypton-85, by the Kety-Schmidt technique. VO2 di was calculated as the product of Q di and the diaphragmatic arteriovenous oxygen difference ([A-V]O2 di). Alteration in these parameters consequent to augmentation of ventilatory effort were compared with concomitant alterations in diaphragmatic electrical activity (EMG di) and an inspiratory pleural pressure-time index (PPTI). Addition of inspiratory resistances combined with inhalation of CO2 usually increased Q di and consistently increased VO2 di, EMG di, and PPTI, the maximum increases being approximately 400-1,600% above control levels. In individual animals, as inspiratory resistance was increased, VO2 di, EMG di, and PPTI rose in direct proportion to each other. In the group as a whole, during resistance breathing the oxygen requirements of the diaphragm were met by a combination of increased [A-V]O2 di and Q di. Unlike other skeletal muscles, oxygen extraction tended to plateau at peak loads, whereas blood flow continued to rise as PPTI and VO2 di increased. We conclude that augmentation of perfusion permits the diaphragm to sustain high levels of contractile effort when the work of breathing is increased.

Diaphragmatic blood flow and energy expenditure in the dog. Effects of inspiratory airflow resistance and hypercapnia.