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Concise Publication Free access | 10.1172/JCI107459
Department of Medicine, University of Oklahoma College of Medicine, Oklahoma City, Oklahoma 73190
Department of Laboratory Medicine, University of Oklahoma College of Medicine, Oklahoma City, Oklahoma 73190
Find articles by Riggs, T. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Oklahoma College of Medicine, Oklahoma City, Oklahoma 73190
Department of Laboratory Medicine, University of Oklahoma College of Medicine, Oklahoma City, Oklahoma 73190
Find articles by Shafer, A. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Oklahoma College of Medicine, Oklahoma City, Oklahoma 73190
Department of Laboratory Medicine, University of Oklahoma College of Medicine, Oklahoma City, Oklahoma 73190
Find articles by Guenter, C. in: JCI | PubMed | Google Scholar
Published October 1, 1973 - More info
It has been postulated that 2,3-diphosphoglycerate (DPG)-mediated changes in oxyhemoglobin affinity play an important role in oxygen delivery; however, the effect of an acute increase in affinity without changing red cell mass has not been systematically evaluated. This study was designed to measure changes in oxygen transport and oxygen consumption produced by an acute increase in oxyhemoglobin affinity caused by an autologous exchange transfusion using DPG-depleted stored blood.
From each of 10 5-kg rhesus monkeys, 100 ml of blood was taken on the 1st and 3rd wk of the study and each stored in 25 ml of acid-citrate-dextrose storage solution. On the 5th wk, each animal underwent an exchange transfusion with 200 ml of its stored blood. Hemodynamic data were obtained before and 30 min after transfusion. The oxyhemoglobin dissociation curve shifted to the left (P50 changed from 33.9 to 27.2 mm Hg), as mean red cell DPG decreased from 28.6 to 12.7 μmol/g of hemoglobin. No significant change was noted in pH, PCO2, base deficit, arterial or venous percent saturation of hemoglobin, cardiac output, or oxygen consumption. However, a fall in mixed venous PO2 from 35.3 to 27.9 mm Hg occurred.
Thus, an acute shift of the oxyhemoglobin curve to the left was accompanied by a significant decrease in the mixed venous PO2 without evidence of acidosis, decreased oxygen consumption, or a compensatory increase in cardiac output.
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