The effect of cardiac disease on hemoglobin-oxygen binding

Woodson, Robert D.; Torrance, J. D.; Shappell, Stephen D.; Lenfant, Claude

doi:10.1172/jci106351

Cited by 117 publications

(36 citation statements)

References 13 publications

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“…The result of a decreased oxygen affinity is a greater oxygen release capacity per gram of circulating hemoglobin, whether this be mediated through increased erythrocyte 2,3-DPG (13,14,18,19), through an intrinsic defect in the hemoglobin molecule producing a low affinity (22), or through increased molecular interaction on deoxygenation, as in Hb SS blood (28). In the erythrocytes of our top fractions the first and third mechanisms are probably operating, but in the high density ISC the low oxygen affinity appears to be due to high hemoglobin concentration alone.…”

Section: Discussionmentioning

confidence: 99%

“…The affinity of adult red blood cells for oxygen is lower than the affinity of solutions of the hemoglobin they contain (14). It is now well established that this effect is due primarily to intracellular organic phosphates (5)(6)(7)(8)(9) of which the most important is 2,3-diphos-phoglycerate (2,3-DPG),7 which acts as a fine regulator of hemoglobin function within the red cell (10).…”

Section: Introductionmentioning

confidence: 99%

“…In a number of dissimilar conditions associated with hypoxemia, an abnormal shift to the right of the red cell oxygen-hemoglobin (02-Hb) equilibrium curve has been observed (11)(12)(13)(14). Many patients with anemia, due to a variety of causes, have a blood oxygen affinity that is lower than normal (15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

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Erythrocyte Hb-S Concentration AN IMPORTANT FACTOR IN THE LOW OXYGEN AFFINITY OF BLOOD IN SICKLE CELL ANEMIA

Seakins¹,

Gibbs²,

Milner³

et al. 1973

J. Clin. Invest.

171

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Erythrocyte Hb-S Concentration AN IMPORTANT FACTOR IN THE LOW OXYGEN AFFINITY OF BLOOD IN SICKLE CELL ANEMIA

Seakins¹,

Gibbs²,

Milner³

et al. 1973

J. Clin. Invest.

171

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“…A decrease in hemoglobin-oxygen affinity (a right-shift of the oxygen dissociation curve (ODC)l has been considered an important physiological adaptive response to conditions in which oxygen transport is impaired, e.g., anemia (1) and myocardial failure (2). Initially, the right-shift found at high altitude (hypoxic hypoxia) was also thought to be an advantageous adaptation (3), but Hebbel et al (4) have shown convincingly that this is not the case.…”

Section: Introductionmentioning

confidence: 99%

Tissue oxygenation and muscular substrate turnover in two subjects with high hemoglobin oxygen affinity.

Wranne¹,

Berlin²,

Jorfeldt³

et al. 1983

J. Clin. Invest.

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A B S T R A C T Oxygen transport to and substrate turnover in leg muscle were studied at rest and during light and heavy upright bicycle exercise in two brothers with a hereditary hemoglobinopathy associated with high oxygen affinity (P50 = 13 mmHg). Femoral venous oxygen tension was below normal and femoral venous oxygen saturation above normal at rest and during exercise. Thus, the arterial-femoral venous oxygen saturation difference was decreased. Despite a compensatory increase in hemoglobin concentration, the arterial-femoral venous oxygen content difference tended to be below normal at heavy exercise. Approximately 25% of the oxygen was delivered via the abnormal hemoglobin at relative heavy exercise. Arterial lactate levels, lactate release, and muscle lactate concentration were not increased at any level of exercise. Glucose, alanine, pyruvate, and glycerol turnover were essentially normal, but the glycogen and creatine phosphate stores were abnormally depleted at the termination of heavy exercise. The exercise electrocardiogram (ECG) was normal, indicating that myocardial oxygenation was adequate. Muscle-surface oxygen pressure fields were normal at rest (not investigated during exercise). It is concluded that the high oxygen affinity of the hemoglobin in our two subjects did not lead to heart or skeletal muscle hypoxia during heavy exercise, as judged from the ECG and from the leg lactate turnover. Despite the lack of evidence for muscle hypoxia, the subjects experienced leg muscle fatigue and the creatine phosphate and glycogen stores were depleted more than normally.

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“…However, all these patients had moderate or severe cardiac disease and under conditions of low cardiac output, P50 values can increase as a compensatory effect. 45 Experimental evidence suggests that methylprednisolone is moderately successful in improving the low P50 and 2,3-DPG present in stored blood,20 and this has been confirmed in a group of patients receiving massive blood transfusion, where the P50 of the methylprednisolone group returned to normal significantly faster than the control group.z1 However, this change with methylprednisolone was not confirmed in patients with burns hock,^ and in studies that have examined P50 and 2,3-DPG, there remains some uncertainty as to whether there is a direct correlation between these m e a~u r e m e n t s~,~~~~~ or n~t .~* '~ In this study we were unable to demonstrate any alteration in the values of P50 and 2,3-DPG that could be attributable to the use of a single large dose of methylprednisolone, and in addition there was no correlation between P50 and 2,3-DPG.…”

Section: Discussionmentioning

confidence: 99%