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1 Department of Physiology, University of Chicago, Chicago, Illinois
By means of chronically implanted vinyl catheters, pressures in aorta, pulmonary artery (PAP), left atrium (LAP), and intrapleural space (by capsule) were recorded simultaneously and continuously, together with cardiac output (Q) by dye-dilution technic every 2 min, in unanesthetized, unsedated trained dogs for 1 hr during breathing of air and low oxygen mixtures (615%) via a chronic tracheostomy. In nearly all of 54 experiments on 5 animals there were striking responses to hypoxia, consisting of a marked rise in PAP (up to 120%), in Q (up to 75%), in pulmonary vascular resistance (PVR) (up to 200%), and of a significant fall in LAP. In some animals these changes were not maintained throughout hypoxia. The PVR usually returned toward normal first, followed by the PAP, while Q remained elevated. The time sequence of these events varied in different animals. Effects of the same magnitude as in hypoxia accompanied restlessness caused by stress, but fluctuated markedly, were of shorter duration, and could largely be climinated by providing quiet surroundings and by avoiding prolonged experiments. It was concluded that active vasoconstriction occurs in the pulmonary vascular bed during acute hypoxia (breathing of 615% O2) in the intact, unanesthetized dog. Furthermore, normal values for PAP, Q, and PVR for the resting, waking dog are reported.
Key Words: cardiac output during acute hypoxia pulmonary artery pressure response to acute hypoxia pulmonary vascular resistance during acute hypoxia
Submitted on June 17, 1963
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