From Bohr‐Haldane Effect on Hb‐O2 Binding to Electrical Regeneration in CHD

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.