Mechanism of Formation of CO2 | Respiration | Humans | Biology

In this article we will discuss about the mechanism of formation of CO₂ with the help of suitable diagrams.

We have seen that hydration of CO₂ occurs in the blood and the mechanism can be represented as CO₂ + H₂O ↔ H⁺+ HCO₃. Further the H⁺ is buffered by reduced Hb within the RBC and by plasma buffers outside the RBC. The reaction can be represented H⁺ + HCO^–₃+ HbO₂↔ HHb + HCO^–₃+ O₂ (liberated in the tissues). HHb represents H ion buffered by reduced Hb).

The negatively charged HCO₃^– left over in the reaction is neutralised by available bases in the blood. The most abundant available base in plasma being Na⁺ the HCO^–₃ in the plasma combines with Na⁺ to form NaHCO₃. The most abundant base within the RBC being K⁺, KHCO₃ is formed in that location. The reaction H₂O + CO₂ ↔ H⁺ + HCO^–₃ is accelerated tremendously due to presence of a specific enzyme carbonic anhydrase within the RBC.

Concentration of HCO^–₃ within the RBC, therefore, becomes very high within a short time and attains a level much higher than that in the plasma. Now since the red cell membrane is impermeable to positively charged ions some HCO^–₃ from within the RBC migrates into plasma and some Cl^– from the plasma migrates within the RBC in exchange of HCO^–₃. This is ailed ‘chloride shift’ phenomenon (Fig. 8.26) and was discovered by Cumburger in 1927. Thus the concentration of HCO^–₃ in plasma becomes higher due to migration of this ion from within the RBC according to the law of Donan’s equilibrium.

(i) CO₂ Transport in the Tissues:

Tension of CO₂ in the tissue fluid is 46 mm Hg (at rest) and that in arterial end of the capillary is 40 mm Hg. CO₂ therefore, diffuses from the tissue space to the capillary due to tension gradient.

It may be recalled that the coefficient of diffusion of CO₂ is very high and in spite of the rather low tension gradient rapid and complete diffusion of CO₂ occurs till tension equilibrium is established.

The H⁺ ion and HCO₃ ion formed are disposed of as follows:

When equilibrium is established the plasma changes may be summarised:

i. Some free molecular CO₂ in solution—which is responsible for CO₂ tension.

ii. Some CO₂ in solution in H₂O as H₂CO.

iii. Some CO₂ buffered as NaHCO₃.

iv. Some CO₂ as carbaminoprotein.

Since formation of H₂CO₃ is accompanied by formation of almost equivalent quantities of NaHCO₃ the ratio H₂CO₃/NaHCO₃ is but little disturbed and the pH of the blood remains almost unaffected.

(ii) CO₂ Transport in the RBC:

CO₂ diffuses rapidly and the reaction CO₂ + H₂O ↔ H₂CO₃ ↔ H⁺+ HCO^–₃ takes place 13,000 times quicker than in plasma because of the presence of the specific enzyme carbonic anhydrase.

Carriage of CO₂ as Carbamino Compound:

CO₂ combines directly with free amino group of the globin and forms carbamino compounds which may be represented as follows:

This occurs:

i. Independent of carbonic anhydrase and therefore the reaction is not inhibited by cynides.

ii. CO₂ is not initially changed to H₂CO₃

iii. At a very rapid rate in the tissues where haemoglobin is desaturated. Carbamino compounds are also formed by direct union of CO₂ with plasma proteins but since the concentration of haemoglobin within the RBC is high, a larger fraction of carbamino compounds are carried within the RBC than in the plasma.

Further an increase in PCO₂ does not increase the formation of carbamino compounds since increased PCO₂ means increased H⁺ concentration which leads to formation HbNH₃⁺. This does not react with CO₂ directly.

Oxygenation of haemoglobin inhibits carbamino compound formation because Oxy-haemoglobin by virtue of its greater acidity H⁺ which blocks carbamino compound formation. Reduced Hb, on the other hand, favours formation of carbino compound.

In the tissues Oxy-Hb is also being converted simultaneously to reduced Hb which is a weaker acid in comparison with the former and has got a weaker hold on the base (K) available within the RBC. If Oxy-Hb is represented symbolically by HbO₂ its ‘salt’ with K (potassium) may be symbolised as KHbO₂. With the ingress of CO₂ and reduction Oxy-Hb the following changes occur.

The KHbO₃, of course, ionises to K⁺ + HCO₃^–. Large quantities of carbamino-haemoglobin are also formed which ionises liberating H⁺ which are neutralised by imidazole group of histadine and β-amino group of valine of the globin polypeptide chains.

As already explained the HCO₃^– from within the RBC is exchanged for CI^– of the plasma according to the law of Donan’s equilibrium (chloride shift). The chloride shift mechanism prevents accumulation of large amount of HCO₃^– within the RBC and thus prevents shifting of its pH to the alkaline side.

(iii) CO₂ Transport in the Lungs (Fig. 8.27):

CO₂ diffuses from plasma (PO₂ = 46 mm Hg) to the alveolar air (PO₂ = 40 mm Hg) and so the H₂CO₃ breaks down liberating further amount of CO₂. Simultaneously oxy-haemoglobin is formed which being a stronger acid snatches off K within the RBC from its combination with acid ions and form KHbO₂. Reversed chloride shift occurs and the HCO^–₃ ion enters the RBC and is broken down liberating further amount of CO₂ which passes from RBC to plasma and then to the lungs.

              

Oxygenation of haemoglobin also breaks down carbamino compound liberating further quantity of CO₂. The mechanism of gas transfer between the lungs → blood → tissues → venous blood and back to the lungs has been summarised in the diagram (Fig. 8.28).