Effect of Oxygen Desaturation from Carbon Monoxide Inhalation on Erythrocytic 2,3-DPG

Erythrocytic 2,3-diphosphoglycerate (2,3-DPG), in response to carbon monoxide (CO) hypoxemia, was studied in 12 rabbits exposed to 250 ppm CO for 3 hours. Each animal served as its own control. Individual determinations of carboxyhemoglobin, arterial oxygen content, oxygen saturation, and 2,3-DPG were made before and immediately after exposures to both CO and normal air. After CO inhalation, there was no significant change in 2,3-DPG despite an average reduction of 22% in arterial oxygen saturation. Moreover, there was no significant correlation between individual oxygen desaturations and changes in 2,3-DPG. The data imply that the 2,3-DPG mechanism offers little or no compensation for this form of hypoxia. OHIO J. SCI. 79(2): 81, 1979 Several causes of hypoxia, such as altitude exposure (Torrance et al 1970), ventilatory impairment (Edwards and Cannon 1972) and anemias (Eaton and Brewer 1968), are associated with increases of 2,3-diphosphoglycerate (2,3DPG) in red blood cells. Since 2,3DPG decreases the affinity of hemoglobin (Hb) for oxygen (Chanutin and Curnish 1967), an increase would shift the oxygen-dissociation curve to the right, promoting tissue oxygenation and thereby offering compensation for the hypoxia. Tobacco smoking and automobiles in modern society have increased the inhalation of carbon monoxide (CO), a common source of induced hypoxia. Studies of the effect of CO exposures on 2,3-DPG have produced varying results. Dinman et al (1970) exposed rats for only 10-15 minutes to high levels of CO. About half the animals showed some increase in 2,3-DPG, whereas the others did not. Astrup (1970) found that 4 of 8 human volunteers reduced their 2,3DPG after a brief CO exposure but the study had no controls. Morena et al (1974) exposed 10 rabbits for 10 minutes to CO (6-13% COHb) and observed a slight mean decrease in 2,3-DPG. RamiManuscript received 6 February 1978 and in revised form 26 June 1978 (#78-8). sey and Casper (1976) found no mean change in 2,3-DPG in 12 rabbits at any 3 hour interval during 24 hours following an exposure producing 20% COHb. In most of the above mentioned studies the exposures were markedly brief, and no assessment was made of the actual O2 deficit. Benesch et al (1968) showed that deoxyhemoglobin binds free 2,3-DPG, thereby stimulating erythrocytic glycolysis to synthesize more. This may explain why subjects at altitude produce more 2,3-DPG. Our study was designed to probe three questions: 1) Do a few hours of CO exposure resulting in 20-25% COHb produce a significant change in 2,3-DPG? 2) How much arterial O2 desaturation results from such exposures? 3) Is there a significant statistical relationship between O2 desaturation and changes in 2,3-DPG? METHODS AND MATERIALS Twelve New Zealand rabbits, weighing 4-5 kg, were selected for the study. They were exposed, one at a time, to normal air for 3 hours in a specially constructed exposure chamber. Blood was withdrawn from the ear artery and the ear vein with needle and syringe before, and immediately after, the 3 hour period. Determinations for Hb content (g/100 ml), COHb (%) and 2,3-DPG (Mmole/ml) were done for each venous sample and O2 content (vol %) was measured from arterial samples. Some of each arterial sample was perfused with 100% O2 in order to measure the full O2 capacity (vol %) . The original O2 content value then was divided