Effects of normobaric hyperoxia on hemodynamics and O2 utilization in conscious dogs.
Normobaric hyperoxia decreased resting whole-body O2 consumption in conscious dogs by equal (Fick) contributions from decreases in cardiac output and in the arterial-venous difference in O2 content. The decrease in O2 consumption was fully developed by 20 min, was maintained for at least 1 h, and was both reversible and reproducible. Hyperoxia also decreased heart rate, right and left ventricular work rates (and therefore, presumably myocardial O2 consumption), and pulmonary vascular resistance; and increased systemic vascular resistance and right atrial pressure. Paradoxically, hyperoxia did not change O2 delivery. This latter observation together with the decrease in O2 consumption produced a unique vertical orientation to the O2 consumption-delivery relationship induced by hyperoxia. It is concluded that hyperoxia may decrease metabolic rate and substantially alter hemodynamics, which may have important implications for understanding the metabolic regulation of oxygen utilization and for the medical and nonmedical uses of oxygen.
Lodato
R F
RF
Division of Pulmonary Medicine and Critical Care, University of Texas Health Science Center, Houston.
D000818:Animals; D002302:Cardiac Output / Q000502:physiology; D004285:Dogs; D005260:Female; D006439:Hemodynamics / Q000502:physiology*; D007700:Kinetics; D008297:Male; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption / Q000502:physiology; D011659:Pulmonary Gas Exchange / Q000502:physiology; D012119:Respiration
D010100:Oxygen