Carbohydrate and lipid metabolism
Under conditions of mitochondrial damage by a phlogistic agent, the efficiency of tissue respiration drops—uncoupling of oxidation and phosphorylation processes occurs. Cells attempt to compensate for the ATP deficiency by activating glycolysis and glycogenolysis. This leads to a massive accumulation of underoxidized products: lactate and pyruvate.
In parallel, during acute inflammation, intensive breakdown of fats is triggered—lipolysis. Lipids are destroyed under the action of released lipases and free radical lipid peroxidation (LPO) reactions. Higher fatty acids (HFAs) accumulate in the tissue, acting as detergents and further damaging biomembranes. However, lipid breakdown products (e.g., arachidonic acid metabolites) become a source of crucial inflammatory mediators—prostaglandins and leukotrienes—while the resynthesis of phospholipids subsequently ensures cell repair.
Protein metabolism disorders
In the focus of acute inflammation, reactions of proteolysis (protein breakdown) dominate over protein synthesis processes.
- Causes: direct destruction of proteins by proteinases, hydrolysis under conditions of tissue acidification (acidosis), and massive release of enzymes from destroyed parenchymal cells and leukocytes.
- Consequences: the accumulation of peptide breakdown products increases oncotic pressure. Denaturation of own protein molecules leads to the formation of autoantigens, which triggers secondary immune reactions. At the same time, the activation of proteolysis is necessary for the destruction of the phlogistic factor itself and the preparation of tissues for subsequent protein resynthesis.
Water-electrolyte imbalance
Cell membrane damage and energy deficiency (decreased ATPase activity) disrupt the function of ion exchangers. A pronounced transmembrane imbalance arises:
| Localization | Accumulating ions |
|---|---|
| Intracellular | Na+, Ca2+ |
| Extracellular | K+, Mg2+ |
The massive release of calcium from mitochondria and the influx of sodium into the cell sharply increase intracellular osmotic pressure. Organelles swell, membranes are 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 causes a cascade of physicochemical shifts in the focus of inflammation:
- Metabolic acidosis: shift of pH to the acidic side due to an excess of underoxidized metabolites. It increases vascular permeability and activates lysosomal enzymes.
- Hyperosmolarity: 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.
- Hyperonquia: increase in protein concentration and their hydrophilicity in the focus, as well as the leakage of albumins from the blood.
- Decrease in surface tension: accumulation of surface-active substances (phospholipids, HFAs) acts as a "lubricant", facilitating cell motility and potentiating adhesion during phagocytosis.
- Liquefaction of the cytoplasm: transition of colloids from a gel to a sol state. The accumulation of Ca2+ ions suppresses the formation of the actin cytoskeleton, which is critical for facilitating phagocyte migration.
Briefly: answers to topical questions
What specific inflammatory mediators directly irritate pain receptors in the focus of alteration?
Pain receptors (nociceptors) in the focus of inflammation are directly irritated by chemical mediators and endogenous algesics.
The main activators include:
- Bradykinin — interacts with pain receptors, causing a sensation of pain;
- Histamine and serotonin;
- Prostaglandins — can independently cause pain and also increase receptor sensitivity to other algesics;
- Substance P (Substance P);
- Potassium ions ($K^+$) and protons ($H^+$);
- ATP.
What enzymes catalyze the conversion of arachidonic acid into prostaglandins and leukotrienes?
The conversion of free arachidonic acid into inflammatory mediators is catalyzed by two main enzymes within corresponding metabolic pathways:
- Cyclooxygenase (COX) — catalyzes the cyclooxygenase pathway, leading to the synthesis of intermediate products from which prostaglandins, prostacyclins, and thromboxanes are formed;
- Lipoxygenase (specifically, 5-lipoxygenase) — catalyzes the lipoxygenase pathway, the end product of which is a distinct group of eicosanoids—leukotrienes.
The rule of three "Hyper"s in the focus of inflammation: Hyperosmolarity (many small molecules), Hyperonquia (lots of protein), and Hyperhydration (lots of water—edema).
Class and exam questions
Why does metabolic acidosis develop in the inflammation focus?
Due to mitochondrial damage, oxidation efficiency decreases, glycolysis is compensatorily activated, and underoxidized products—lactate, pyruvate, as well as higher fatty acids and amino acids—accumulate in tissues.
How and why does the colloidal state of the cytoplasm change?
A transition from a gel to a sol state (liquefaction) occurs. This is associated with the accumulation of calcium ions, which suppress the polymerization of the actin cytoskeleton. Such a shift facilitates the migration of phagocytes to the site of inflammation.
What is the cause of pain during metabolic shifts?
Pain syndrome in the primary alteration zone arises due to hyperosmolarity, hyperonquia, accumulation of inflammatory mediators, and the direct irritating effect of the acidic environment (acidosis) on receptors.
What else to study on this topic
- Mechanisms of inflammatory mediator formation from arachidonic acid
- The role of free radical lipid peroxidation (LPO) in membrane destruction
- Electrophysiological disturbances and depolarization of cardiomyocyte membranes
- The effect of surface-active substances on phagocytosis and adhesion processes
- Mechanisms of cell surface charge alteration and electrogenesis disorders
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