Abstract
AIMDespite extensive clinical and basic research, the precise mechanism for Hb‐O2 binding remains to be determined. Since we have confirmed that ↑RBC K rapidly reverses angina, ST‐T alterations, and induces electrical regeneration of heart in CHD, we tested the hypothesis that RBC K transport is involved on Hb‐O2 binding in human RBC.Methods/SubjectsHeparin venous sample from healthy subjects were analyzed before (4 ml) and after in Vitro oxygenation (4 ml +1ml 100% O2). In all pH, PO2/PCO2, HCO3 (Stat Profile pHOx), RBC/plasma electrolytes (Na, K, Atomic Emission Spectrophotometry), Cl (Lytek‐Cl). Statistical using Student's t‐test, analysis of variance, p<0.05 as exponential values.ResultsIn Vitro blood oxygenation (O2 Sat 87±3 vs 47±6%) resulted in sharply ↓ RBC Ki (87.6± 2.3 vs 92.0±2.3 mmol/lcell, p<4.5E‐09), ↓ RBC Nai (5.8±0.2 vs 6.3±0.2 mmol/lcell, p<6.5E‐05) along with ↓ plasma K (3.3 ±0.3 vs 3.8±0.2 mmol/l, p<9.7E‐05), ↓ Na (134±4 vs 139±2.2, p<1.3E‐03) and ↓ Cl (91±1.6 vs 98.3±1.2 mmol/l, p<7.9E‐11), uncovering a complex biochemical event in Hb‐O2 binding and Bohr Effect, which excludes a simple gas diffusion.ConclusionThis observation strongly support our novel therapeutic approach improving RBC K, and probably myocardial O2 transport in CHD. Second, it is proposed that RBC K exchange should be included in evaluation of Bohr‐Haldane Effects in clinical and experimental human Hb‐O2 exchanges.
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