General Characteristics and Dynamics of the Process
Plasma inflammatory mediators represent a complex of biologically active substances. They circulate in the bloodstream as inactive precursors, are activated by specific triggers, and are strictly controlled by inhibitors. The primary feature of this group is their function via a cascade mechanism, where the activation of a single molecule triggers a chain reaction of subsequent components.
In the dynamics of the inflammatory process, plasma factors do not come into play immediately. The strict sequence is as follows: first, cellular mediators are released in the tissues, provoking a primary vascular response, and only then are plasma mediators recruited. This leads to a massive influx of exudate into the lesion.
The global goal of all these reactions boils down to three tasks: reliable demarcation of the site of injury, immobilization of the pathogenic factor within it, and its eventual destruction.
Basic Effects of Plasma Systems:
- Marked increase in microvascular permeability.
- Recruitment of monocytes and polymorphonuclear leukocytes to the lesion (chemotaxis).
- Stimulation of phagocytosis.
- Initiation of intravascular coagulation.
Kinin System
The components of this system are derived from blood plasma and other body fluids. Key representatives include kinins (specifically kallidin and bradykinin), as well as the enzyme kallikrein.
- Bradykinin exhibits a marked hypotensive effect (lowering blood pressure) and causes arteriolar dilation. It is directly responsible for generating the sensation of pain at the site of inflammation. In addition, it dramatically enhances vascular permeability, stimulates collagenogenesis, and activates the enzyme cyclooxygenase.
- Kallikrein plays a crucial linking role. Its primary significance lies in activating the Hageman factor, thereby directly integrating the blood coagulation and fibrinolytic systems into the inflammatory response. Kallikrein also mediates targeted leukocyte chemotaxis and stimulates phagocytes.
Complement System
The complement system consists of specific plasma proteins synthesized by hepatocytes, monocytes, and leukocytes. The primary function of complement is bactericidal activity and cytolysis, i.e., the direct destruction of bacteria and cells (including the lysis of damaged host tissues).
Key components of the system, particularly the C3b and C5b fractions, elicit a wide range of effects:
- Potent opsonization (preparing foreign particles for uptake by phagocytes).
- Enhancement of chemotactic activity and adhesion of macrophages, neutrophils, and other leukocytes.
- Dilation of the capillary network and a significant increase in microvascular permeability.
- Additional stimulation of lipoxygenase and cyclooxygenase enzymes.
- Activation of the Hageman factor, further demonstrating the close interdependence of all three plasma systems.
Hemostatic System and Hageman Factor
The components of the blood coagulation system are produced in the liver. During inflammation, the hemostatic system becomes an integral component of the reaction rather than merely a mechanism for arresting hemorrhage.
The central link here is Factor XII (Hageman factor). It initiates blood clotting and acts as a potent inflammatory mediator:
- Activates other plasma mediators (including the kinin system).
- Increases vascular wall permeability.
- Enhances neutrophil migration into the lesion.
- Stimulates platelet aggregation.
As a result of hemostatic system activity, microthroμβι form, physically blocking the spread of infection. Subsequently, fibrin clot lysis is triggered, leukocyte adhesion is enhanced, and fibroblast proliferation begins, preparing the tissue for regeneration.