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* Haldane: role of oxygen, either loading or unloading, Hb release proton, change the capacity of (necessary converse of Bohr effect) Bohr, proton kicks out oxygen (in tissue; reversal Bohr-Haldane-in lung) Haldane, oxygen * Reverse Bohr effect (oxygen ? CO2; CO2 ? oxygen) @ lung: Up (uptaking) O2 ? promotes unloading CO2 at lungs @ tissue: Down (releasing) O2 ? promotes loading CO2 at tissue O2 effects the buffering capacity of Hb-ability to bind protons (H+) * Haldane effect Imidazole (Im) groups on Hb take up H+ in their role as buffers (increased affinity when Hb is deoxygenated) Carbonic anhydrase in the RBC catalyzes this reaction Some bicarbonate buffered in the RBC is carried inside the RBC, but most diffuses out of the RBC via the rapid anion exchange protein. This bicarbonate is carried in the plasma, although buffered in the RBC. Bicarbonate produced in the plasma is buffered by plasma protein (Pr) * Electric change varies with temperature Eg. When temperature falls, pK of Im increase, affinity to combine with H+; to opposite, decreasing H2 concentration, raising pH! Accordingly, it helps prevent the proportion of positively charged groups on proteins from changing. * * * Respiratory disturbance of pH: altering blood property initially on PCO2 Metabolic disturbance of pH, initially alter the blood bicarbonate concentration * In very high O2 environment, not need to have a lot Hb (left daphria) Grown in low O2 environment, more Hb in the right daphria * PO2 is the driving force to uptake O2 At saturation, 4 molecules of O2 in one Hb in high PO2 (From left graph to right) Carrying capacity 20 mL of oxygen per 100mL of blood when carrying 100% saturation of Hb So 90% of oxygen in the blood bind to Hb Increase uptake O2 by 50 times in blood * [#] is the # of Oxygen on Hb At high PO2, flat %Hb uptake, need fairly large change to have Hb uptake O2 In contrast, at low PO2, the curve is pretty steep, only takes a little change in PO2 to change saturation
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