CO2 Transport in Blood

Carbon dioxide (CO2) is the end-product of energy metabolism p. 228). CO2 produced by cells of the body undergoes physical dissolution and diffuses into adjacent blood capillaries. A small portion of CO2 in the blood remains dissolved, while the rest is chemically bound in form of HCO3- and carbamate residues of hemoglobin (^ A , lower panel, blue arrows; ^ arteriovenous CO2 difference given in the table). Circulating CO2-loaded blood reaches the pulmonary capillaries via the right heart. CO2 entering the pulmonary capillaries is released from the compounds (^ A, red arrows), diffuses into the alveoli, and is expired into the atmosphere (^ A and p. 106).

The enzyme carbonic anhydrase (carbonate dehydratase) catalyzes the reaction

HCO3- + H+ CO2 + H2O in erythrocytes (^ A5, 7). Because it accelerates the establishment of equilibrium, the short contact time (< 1 s) between red blood cells and alveolus or peripheral tissue is sufficient for the transformation CO2 HCO3-.

CO2 diffusing from the peripheral cells (^ A, bottom panel: "Tissue") increases Pco2 (approx. 5.3 kPa = 40 mmHg in arterial blood) to a mean venous Pco2 of about 6.3 kPa = 47 mmHg. It also increases the concentration of CO2 dissolved in plasma. However, the major portion of the CO2 diffuses into red blood cells, thereby increasing their content of dissolved CO2. CO2 (+ H2O) within the cells is converted to HCO3- (^ A5,2) and hemoglobin carbamate (^ A3). The HCO3-concentration in erythrocytes therefore becomes higher than in plasma. As a result, about three-quarters of the HCO3- ions exit the erythrocytes by way of an HCO3/Cl- antiporter. This anion exchange is also called Hamburger shift (^ A4).

H+ ions are liberated when CO2 in red cells circulating in the periphery is converted to HCO3- and hemoglobin (Hb) carbamate. Bicarbonate formation: CO2 + H2O HCO3+ H+, [5.4]

Hemoglobin carbamate formation: Hb-NH2 + CO2 Hb-NH-COO- + H+. [5.5] Hemoglobin (Hb) is a key buffer for H+ ions in the red cells (^ A6; see also p. 140, "Non-bicarbonate buffers"). Since the removal of H+ ions in reactions 5.4 and 5.5 prevents the rapid establishment of equilibrium, large quantities of CO2 can be incorporated in HCO3- and Hb carbamate. Deoxygenated hemoglobin (Hb) can take up more H+ ions than oxygenated hemoglobin (Oxy-Hb) because Hb is a weaker acid (^ A). This promotes CO2 uptake in the peripheral circulation (Haldane effect) because of the simultaneous liberation of O2 from erythrocytes, i.e. deoxygenation of Oxy-Hb to Hb.

In the pulmonary capillaries, these reactions proceed in the opposite direction (^ A, top panel, red and black arrows). Since the Pco2 in alveoli is lower than in venous blood, CO2 diffuses into the alveoli, and reactions 5.4 and 5.5 proceed to the left. CO2 is released from HCO3- and Hb carbamate whereby H+ ions (released from Hb) are bound in both reactions (^ A7, A8), and the direction of HCO3 /Cl- exchange reverses (^ A9). Reoxygenation of Hb to Oxy-Hb in the lung promotes this process by increasing the supply of H+ ions (Haldane effect).

CO2 distribution in blood (mmol/L blood, 1 mmol = 22.26 mL CO2)






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