Carbohydrate and Lipid Metabolism
Under conditions of mitochondrial damage by a phlogistic agent, the efficiency of tissue respiration drops—uncoupling of oxidation and phosphorylation occurs. Cells attempt to compensate for the ATP deficit by activating glycolysis and glycogenolysis. This leads to a massive accumulation of under-oxidized products: lactate and pyruvate.
In parallel, acute inflammation triggers intense fat breakdown—lipolysis. Under the action of released lipases and free radical lipid peroxidation (LPO) reactions, lipids are destroyed. Free fatty acids (FFAs) accumulate in the tissue, acting as detergents and further damaging biomembranes. However, lipid breakdown products (such as arachidonic acid metabolites) become the source of crucial inflammatory mediators—prostaglandins and leukotrienes—while phospholipid resynthesis subsequently ensures cell repair.
Protein Metabolism Disorders
In the focus of acute inflammation, proteolysis (protein breakdown) reactions dominate over protein synthesis processes.
- Causes: direct destruction of proteins by proteinases, hydrolysis under conditions of medium acidification (acidosis), and a massive release of enzymes from destroyed parenchymal cells and leukocytes.
- Consequences: the accumulation of peptide breakdown products increases oncotic pressure. Denaturation of endogenous protein molecules leads to the formation of autoantigens, which triggers secondary immune reactions. At the same time, the activation of proteolysis is necessary to destroy the phlogistic factor itself and prepare tissues for subsequent protein resynthesis.
Water-Electrolyte Imbalance
Cell membrane damage and energy deficits (decreased ATPase activity) disrupt the function of ion exchangers. A pronounced transmembrane imbalance develops:
| Localization | Accumulating Ions |
|---|---|
| Intracellular | Na+, Ca2+ |
| Extracellular | K+, Mg2+ |
Massive calcium efflux from mitochondria and sodium influx into the cell sharply increase intracellular osmotic pressure. Organelles swell, membranes become overstretched, which inevitably leads to cell death. Tissue hyperhydration (edema) develops, and persistent membrane depolarization disrupts the functions of excitable cells.
Physicochemical Changes
The metabolic catastrophe triggers a cascade of physicochemical shifts in the inflammation focus:
- Metabolic acidosis: shift of pH toward the acidic side due to an excess of under-oxidized metabolites. It increases vascular permeability and activates lysosomal enzymes.
- Hyperosmolality: increase in osmotic pressure due to the enzymatic cleavage of large molecules (glycogen, proteoglycans) into small fragments and the release of osmotically active substances from dead cells.
- Hyperoncria: increase in protein concentration and their hydrophilicity in the focus, as well as the leakage of albumins from the blood.
- Decreased surface tension: accumulation of surface-active substances (phospholipids, FFAs) acts as a "lubricant," facilitating cell mobility and potentiating adhesion during phagocytosis.
- Liquefaction of the cytoplasm: transition of colloids from a gel to a sol state. Accumulation of Ca2+ ions suppresses actin lattice formation, which is critical for facilitating phagocyte migration.