Mechanism of microbial fever
When infectious agents invade brain tissues, the production of a specific endogenous pyrogen—interleukin-1 (IL-1)—is activated. This substance directly acts on the thermoregulatory centers in the hypothalamus, causing a functional restructuring:
- The excitability of nerve cells sensitive to cold increases significantly.
- At the same time, the impulse activity of neurons reacting to heat decreases.
The key molecular mediators in this chain are arachidonic acid derivatives (primarily prostaglandins of the E group), as well as adrenocorticotropic hormone (ACTH). As a result, the body begins to perceive its normal temperature as too low and triggers heat production mechanisms.
Hyperthermia and consequences of overheating
If the ambient temperature rises above the blood temperature, the body begins to passively heat up. Excess heat enters the body through heat radiation and thermal conduction processes.
In response to hyperthermia, compensatory reactions are triggered. A human experiences tachycardia (rapid heart rate) and tachypnea (rapid breathing). In animals, such as dogs, cooling occurs via polypnea—very rapid breathing that repeatedly enhances the evaporation of saliva from the surface of the respiratory mucosa.
Prolonged exposure to high temperatures leads to the exhaustion of compensatory mechanisms:
- Respiratory alkalosis occurs (as a result of pronounced hyperventilation).
- Heat stroke develops, accompanied by profound CNS depression and loss of consciousness.
Artificial hypothermia in clinical practice
Unlike overheating, artificial body cooling is widely used in medicine. Hypothermia implies the targeted reduction of core body temperature to 29–30 °C. The main physiological purpose of the procedure is a sharp slowdown of all metabolic processes in tissues, putting cells into a state of hypo- and anabiosis.
This technique is indispensable in cardiac surgery: it allows complex operations to be performed on a "dry" heart temporarily excluded from blood circulation, significantly increasing the allowable ischemia time.
Methods for achieving hypothermia:
- Physical cooling (immersion in ice water, ice packing). The main disadvantage of the method is the development of severe cold stress, which exhausts the body.
- Chemical (pharmacological) hypothermia. Considered the most effective. Prior pharmacological blockade of the heat production center prevents the stress reaction to cold before cooling begins.
V.M. Bakhmetiev's theory of anabiosis
Prospects for studying temperature effects are inextricably linked with the doctrine of anabiosis, founded by V.M. Bakhmetiev. The core idea of the theory is the ability to arbitrarily stop and then restart cellular metabolism (following the principle of a mechanical clock pendulum).
Beyond medicine, the management of anabiosis is of colossal interest to cosmonautics. The introduction of controlled anabiosis technologies in long-term space flights will radically reduce the required food supply volumes.
Briefly: answers to topical questions
What stages are distinguished in the pathogenesis of a typical fever?
Three successive stages are distinguished in the pathogenesis of a typical fever.
- Temperature rise (stadium incrementi) — caused by a shift in the ratio between heat production and heat loss.
- Temperature plateau (stadium fastigii) — the stage of elevated temperature.
- Temperature decrease — return of body temperature to the normal range.
What mechanisms of physical thermothermoregulation are activated in humans during hyperthermia?
At high ambient temperatures, physical thermoregulation (heat loss) mechanisms are activated to dissipate heat.
- Sudomotor response — sweating and evaporation of moisture from the skin surface.
- Vasomotor response — vasodilation (dilation) of skin blood vessels, increasing heat loss via radiation and convection.
- Respiratory response — the intensity of external respiration increases (breathing rate increases).
- Piloerection change — the arrector pili muscle (m. arrector pili) relaxes, and hairs lie flat against the skin.
How does the development mechanism of fever fundamentally differ from hyperthermia?
The fundamental difference is that fever is a protective adaptive reaction, whereas hyperthermia is a pathological process resulting from the breakdown of thermoregulation mechanisms.
| Criterion | Fever | Exogenous hyperthermia |
|---|---|---|
| Cause | Pyrogens | High ambient temperature |
| Key mechanism | Temporary dynamic restructuring of the thermoregulatory system (shift of the “set point”) | Failure of the body's adaptation mechanisms to the action of exogenous heat |
| Diurnal variations | Preserved | Absent |
Which classes of pyrogens are distinguished based on their origin?
Depending on their origin, pyrogens are divided into two main groups.
- Primary pyrogens — a heterogeneous group of substances of exogenous or endogenous origin (e.g., lipopolysaccharides) that induce the synthesis of secondary pyrogens.
- Secondary pyrogens — endogenous cytokines (e.g., interleukin-1) produced by leukocytes under the action of primary pyrogens, triggering the febrile response.
To easily remember the action of interleukin-1 during a fever, imagine how climate control works: it "turns on the heater" (exciting cold neurons, forcing the body to warm up) and "turns off the air conditioner" (inhibiting heat neurons).
Class and exam questions
Why can alkalosis develop during hyperthermia?
In response to overheating, rapid breathing (tachypnea) occurs. Prolonged hyperventilation leads to the excessive removal of carbon dioxide from the blood, shifting the acid-base balance toward the alkaline side.
Why is pharmacological blockade used when cooling a patient?
Exclusively physical ice cooling causes the patient a powerful protective cold stress. Drug blockade of the heat production center suppresses this undesirable reaction.
What role do prostaglandins E play in fever?
These arachidonic acid metabolites act as key molecular mediators transmitting the pyogenic signal from interleukin-1 to hypothalamic neurons.
What else to study on this topic
- Arachidonic acid metabolism cascade in thermoregulation
- Differences between polypnea in animals and tachypnea in humans
- Pathogenesis of loss of consciousness during heat stroke
- Effect of adrenocorticotropic hormone (ACTH) on temperature homeostasis
- Cellular and biochemical mechanisms of hypobiosis
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