NaH2PO4 + NaCl = Na2HPO4 + HCl.
It is also to be noted that the disodium hydrogen phosphate, may, likewise, give rise to hydrochloric acid through its action on calcium chloride, as indicated by the following equation:
2Na2HPO4 + 3CaCl2 = Ca3(PO4)2 + 4NaCl + 2HCl.
It is thus evident that hydrochloric acid may originate in the inter-reaction of these several salts which are known to be present in the blood; but obviously, the above reactions cannot take place in the blood itself, and we must look to the selective power of the epithelial cells of the gastric glands, as suggested by Gamgee,[96] for the withdrawal of the needed salts from the blood. Once present in the acid-forming cells, and perhaps aided by the inherent qualities of the protoplasm, the necessary chemical reactions may be assumed to take place, after which the newly formed acid may pass from the gland-cells into the secretion of the gland.
A later theory regarding the formation of the acid of the gastric juice emanates from Liebermann.[97] This investigator claims the existence in the mucous membrane of the stomach of an acid-reacting, nuclein-like body, which is apparently a combination of the phosphorized substance lecithin with a proteid. To this compound body Liebermann gives the name of lecithalbumin. It is apparently located in the nuclei of the gastric cells, is strongly acid in reaction, and, according to Liebermann, is an important agent in the production of the free hydrochloric acid of the gastric juice, although its action is somewhat indirect. According to this theory, the free acid is formed in the mucous membrane of the stomach from sodium chloride, through the dissociating action of the carbonic acid coming from normal oxidation. The thus-formed acid then diffuses in both directions, viz., through the lumen of the gland into the stomach-cavity, and in part in the opposite direction into the veins and lymphatics. It is the assumed function of the lecithalbumin to react with the alkaline sodium carbonate, produced simultaneously with the hydrochloric acid. This naturally gives rise to the liberation of carbonic acid and to the formation of a non-diffusible sodium-lecithalbumin compound, which is retained for the time being in the body of the cell. When the circulation of the blood, accelerated by the digestive process, returns to its ordinary pace, this latter compound is slowly decomposed by the carbonic acid with formation of the readily diffusible sodium carbonate, which passes into the blood-current. The rate of this latter reaction is impeded, or, perhaps regulated, by the swelling up of the lecithalbumin-containing cells, thus rendering the imbibition of the carbonic acid a slow process. The rate of production of the hydrochloric acid by this hypothetical process depends primarily upon the blood supply, and the oxidative changes by which carbonic acid is formed.
There is much that might be said for and against this theory,[98] but we cannot stop to discuss it here. Like the previous theory, it implies the production of hydrochloric acid from a chloride or chlorides, through chemical processes taking place in the stomach-mucosa, and presumably in the large border-cells of the peptic glands. This hydrochloric acid, as you know, in the act of secretion, reacts upon the pepsinogen with which it may come in contact, transforming it into pepsin. It also has the power of combining with all forms of proteid matter, not excepting the products of proteolytic action, to form acid compounds in which the so-combined acid, although equal quantitatively to the original amount of free acid, is less active in many ways. Thus, it does not possess in the same degree a destructive action on the amylolytic ferments;[99] it does not play the same part in aiding the proteolytic action of pepsin, and its antiseptic power is far from equal to that of a like amount of free acid.[100]
With relatively large amounts of proteid, we may have half or even quarter saturated proteid molecules, in which the weakness of the combined acid is far more pronounced than in the case of the fully saturated molecule. Such a condition of things must obviously exist in the early stages of gastric digestion. With an excess of proteid matter in the stomach, some time must elapse before the secretion of hydrochloric acid will be sufficient to furnish acid for all of the proteid matter present, yet pepsin-proteolysis does not wait the appearance of free acid. Indeed, the proteid matter may not have combined with more than half its complement of hydrochloric acid before digestive proteolysis is well under way. I have made many analyses of the stomach-contents after test meals, and under other conditions, where no free acid could be detected by the tropaeolin test, or better, by Günzburg’s reagent (phloroglucin-vanillin), although phenolphthalein as well as litmus showed strong acid reaction, and yet not only could acid-albumin be detected in the filtered fluid, but likewise proteoses and peptones. In other words, pepsin-proteolysis can proceed in the absence of free hydrochloric acid, although not at the same pace. Hence, proteoses and even peptones may make their appearance in the stomach-contents at a very early period of digestion, i. e., the final products of proteolysis may be found in a mixture containing even a large proportion of wholly unaltered proteid, and obviously at an early stage in the process. Expressed in other language, a portion of the first formed acid-albumin or syntonin may be carried forward by the digestive process to the secondary proteose and peptone stage, before the larger portion of the ingested proteid food has even combined with sufficient acid to insure the complete formation of acid-albumin. This introduces another factor, to be referred to later on, viz., the relative combining power of different forms of proteid matter, especially the proteoses and peptones, as contrasted with native proteids.
In proof of the statement that pepsin-proteolysis can proceed in the absence of free hydrochloric acid, provided combined acid be present, allow me to cite one or two experiments bearing on this point. A perfectly neutral solution of egg-albumen, containing 0.8169 gramme of ash-free albumin per 10 c.c. of fluid, was employed as the proteid material. In order to completely saturate the proteid contained in 20 c.c. of this neutral albumen solution, 50 c.c. of 0.2 per cent. HCl were required. Two mixtures were then prepared as follows:
A. Twenty c.c. of the neutral albumen solution + 50 c.c. 0.2 per cent. HCl + 30 c.c. of a weak aqueous solution of pepsin, perfectly neutral to litmus. This mixture gave only the faintest tinge of a reaction for free acid when tested by Günzburg’s reagent.