Physiology of Gastric Secretion and Protection
Hydrogen ion secretion is carried out by parietal cells. This process is regulated by central nervous system pathways and humoral factors. The main stimulation pathways include neuronal (acetylcholine via the vagus nerve), paracrine (histamine), and humoral (gastrin). The basolateral membrane of the cell features corresponding receptors: M3 muscarinic receptors, H2 histamine receptors, and CCK2 receptors.
The intracellular signaling cascade culminates in the activation of the H+, K+-ATPase enzyme ("proton pump"). It transports protons into the gastric lumen in exchange for potassium ions, establishing a massive gradient: the intracellular pH is 7.8, while the extracellular pH drops to 0.8.
Mucosal defense (gastroprotection) is provided by mucus (hydrophilic glycoproteins), bicarbonate secretion, and robust blood flow that washes away penetrated hydrogen ions. The primary regulators of defense are prostaglandins E2 and I2, which stimulate mucus production and inhibit acid secretion.
Classification of Antacids
Antacids are divided into three main groups based on their systemic absorption and mechanism of action:
- Absorbable (systemic): sodium bicarbonate (baking soda), calcium carbonate, magnesium oxide, and magnesium carbonate.
- Non-absorbable (non-systemic): algeldrate, magnesium trisilicate, and combination products (Almagel, Maalox).
- Adsorbents: bismuth subnitrate and related preparations (Vikalin, Vikair).
The standard dose for powder formulations is 0.5–1.0 g. They must be dissolved in half a glass of water before administration.
Absorbable Agents: Characteristics and Drawbacks
Sodium bicarbonate is the fastest-acting agent, but it has severe drawbacks. The acid neutralization reaction is accompanied by vigorous carbon dioxide evolution. The gas distends the gastric walls, which triggers a secondary increase in secretion ("rebound" syndrome). Furthermore, frequent administration causes systemic alkalosis.
Calcium carbonate (precipitated chalk) has moderate efficacy. It also releases carbon dioxide, causing eructation and flatulence. The calcium chloride formed during the reaction is absorbed into the bloodstream, and the drug itself has a pronounced antidiarrheal effect that can lead to constipation.
General side effects of antacids include decreased appetite and dyspeptic disorders (belching, vomiting).
Non-Absorbable and Combination Agents
Magnesium preparations (magnesium oxide) neutralize acid without gas formation and act more effectively than sodium bicarbonate. Upon reaching the intestine, they exert a laxative effect. Magnesium trisilicate works slowly: it forms a colloid that coats and protects the mucosa from pepsin and acid.
Aluminum preparations (algeldrate) also do not produce gas and possess adsorbent properties, but they cause constipation.
To balance the side effects on intestinal motility, combination drugs were developed:
- Almagel (aluminum + magnesium + D-sorbitol) is available as a gel for uniform mucosal distribution. It exerts choleretic and laxative effects. The Almagel A modification additionally contains anestesin to relieve pain and nausea.
- Maalox (aluminum + magnesium + sorbitol + mannitol) possesses a unique cytoprotective property. It stimulates the synthesis of prostaglandin E2, increasing the production of protective mucus.
Systemic Risks of Aluminum Preparations
Prolonged use of non-absorbable, aluminum-containing antacids leads to specific metabolic disturbances. In the small intestine, insoluble aluminum phosphate salts are formed, completely blocking the absorption of dietary phosphates.
Clinically, phosphate deficiency manifests as weakness, malaise, and impaired vitamin D3 synthesis. In severe cases, osteoporosis, renal impairment, and encephalopathy (brain damage) develop. Due to these risks, the treatment course with aluminum-containing drugs is strictly limited and should not exceed two weeks.