Many cases with vascular dementia have multiple lacunaes and diffuse demyelination in the white matter (vascular leukoencephalopathy; VLE). One of the major causes of VLE is chronic hypoxia. 2, 3-diphosphoglycerate (DPG) in red cells plays an important role in oxygen delivery in microcirculation. It decreases the oxygen affinity of hemoglobin and facilitates the unloading of oxygen from hemoglobin, displacing the oxygen dissociation curve to the right. In this study red cell DPG and P
50 (P
O2 at half saturation) in demented patients with VLE were compared with those in non-demanted, post-stroke patients (NDPS) who had localized brain lesions and in control cases. The results were as follows. 1) DPG was inversely proportional to hemoglobin concentration. DPG levels were significantly elevated in NDPS patients compared with controls, but was not different between VLE patients and controls. 2) P
50 was inversely proportional to hemoglobin concentration. P
50 was significantly reduced in VLE patients, but was not different between NDPS patients and controls 3) P
50 was proportional to DPG levels. VLE patients had significantly lower P
50 than controls, while P
50 was different between NDPS and controls. The results suggest that DPG and P
50 are compensatorily elevated in non-demented post-ischemic patients, while such compensation is lacking in demented patients with vascular leukoencephalopathy. In such demented patients the red cell oxygen affinity which causes tissue hypoxia has a tendeny to increase above the normal level. Decompensation of red cell DPG synthesis may have an important implication in the pathogenesis of vascular leukoencephalopathy.
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