Advertisement
Research Article Free access | 10.1172/JCI106351
Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98105
Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, Washington 98105
Find articles by Woodson, R. in: PubMed | Google Scholar
Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98105
Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, Washington 98105
Find articles by Torrance, J. in: PubMed | Google Scholar
Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98105
Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, Washington 98105
Find articles by Shappell, S. in: PubMed | Google Scholar
Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98105
Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, Washington 98105
Find articles by Lenfant, C. in: PubMed | Google Scholar
Published July 1, 1970 - More info
The relation between degree of cardiac functional impairment and changes in hemoglobin-oxygen affinity and 2,3-diphosphoglycerate (2,3-DPG) has been studied in 39 patients with noncyanotic heart disease. A progressive decline in hemoglobin-oxygen affinity was found with worsening cardiac function as assessed by cardiac index, arteriovenous oxygen (A-V O2) difference, and cardiac symptoms; this alteration in hemoglobin-oxygen binding represents a significant mechanism for adaptation to the limited oxygen supply imposed by the cardiac lesion. The highly significant correlation of mixed venous blood oxygen saturation (S[unk]VVO2) with 2,3-DPG and the position of the oxygen dissociation curve suggests that the level of deoxygenated hemoglobin is an important in vivo regulator of hemoglobin-oxygen affinity.