What are the vasoactive substances in inflammatory mediators 4 are sufficient .

Thromboxane A2, histamine, serotonin, bradykinin.

Angiotensin L, epinephrine, norepinephrine, endothelial relaxation factor (such as nitric oxide) and endothelin, vasopressin, atrial natriuretic peptide, kinin, histamine, prostaglandin, opioid peptide are currently known.

The basic pathological changes of inflammation include alteration, exudation, and proliferation.

1. Deterioration: degeneration and necrosis of local tissues due to inflammation.

2. Exudation: the process by which the fluid and cellular components in the blood vessels of the local tissues of the inflammation enter the interstitium, body cavity, mucosal surface and body surface through the blood vessel wall. Exudation is the most characteristic change in inflammation.

1. Hemodynamic changes. 2. Increased vascular permeability. (1) Endothelial cell contraction.

2) Endothelial cell damage. (3) High permeability of new capillaries. 3. The role of exudate:

Local inflammatory edema dilutes toxins and reduces the damaging effect of toxins on the local; Brings nutrients and metabolites to locally infiltrated leukocytes; The antibodies and complement contained in the exudate favor the destruction of pathogens; The fibrin formed by fibrinogen in the exudate is interwoven into a web, which restricts the diffusion of pathogenic microorganisms, is conducive to leukocyte phagocytosis and destroys pathogens. The pathogenic microorganisms and toxins in the exudate are carried to the local lymph nodes along with the lymph, which is conducive to the production of cellular and humoral immunity. Excess exudate has a compressive and blocking effect, and cellulose in the exudate can be organized if malabsorption. 4. Exudation and phagocytosis of leukocytes. (1) Leukocyte edge set.

2) Leukocyte adhesion. (3) Leukocyte efflux and chemotactic effects. (4) Local role of leukocytes:

Phagocytosis, immunity, tissue damage. 5. The role of inflammatory mediators in the inflammatory process (1) Inflammatory mediators released by cells: vasoactive amines (histamine and serotonin), arachidonic acid metabolites, leukocyte products, cytokines and chemical factors, platelet activating factor, NO and neuropeptides.

2) Inflammatory mediators in body fluids: kinin system, complement system, coagulation system, fibrinolytic system.

3. Proliferation: including the proliferation of parenchymal cells (such as nasal mucosal epithelial cells and glandular cells) and mesenchymal cells (macrophages, vascular endothelial cells, fibroblasts).

The basic pathological changes in inflammation are copied as follows: BAI

1.Deterioration: Inflammation occurs locally in tissues

The degeneration and necrosis of the degeneration is called metamorphosis

Metamorphosis can occur in both parenchymal DAO cells and mesenchymal cells. Common metamorphic changes in parenchymal cells include cell edema, steatosis, apoptosis, coagulative necrosis, and liquefaction necrosis. Common metamorphic changes in interstitial cells include mucinous degeneration and fibrinous necrosis.

2.Exudation: The process by which fluid components in blood vessels, proteins such as cellulose and various inflammatory cells in the blood vessels of the inflammatory local tissues enter the interstitial space, body cavity, body surface, or mucosal surface through the blood vessel wall is called exudation.

The process of exudation can be summarized as consisting of three interrelated events: (1) changes in vessel caliber and increased blood flow (inflammatory congestion); (2) increased vascular permeability (inflammatory effusion); (3) White blood cell outflow and aggregation (inflammatory infiltration).

Exudation is caused by a series of local hemodynamic changes, increased vascular permeability, and active leukocyte efflux and phagocytosis activity, which is an important marker of inflammation and has an important defensive role in the local area.

The biological functions of the complement system include inflammatory mediators, bactericidal effects, immune effects, opsonization effects, viral effects, etc., most of which are exerted by various active substances (mainly cleavage products) produced during the activation of the complement system.

Bactericidal effect, complement can dissolve red blood cells, white blood cells and platelets. Complement can also lyse or kill certain gram-negative bacteria; Opsonization, where the complement cleavage product C3B binds to bacteria or other particles and promotes phagocytosis of phagocytes, which is called complement opsonization.

Immunity, after the immune complex activates complement, it can adhere to red blood cells, platelets, or certain lymphocytes with C3B receptors on the surface through C3B, forming a larger polymer that may help to be engulfed and cleared; Viral action, in which complement is added to the complex formed by the virus and the corresponding antibody, the neutralizing effect of the antibody on the virus is significantly enhanced, and the adsorption and penetration of the virus into the host cell are prevented.

1.Lyse target cells in all types of cells with enveloped viruses2Promotes phagocytosis of kinin-like effects

C2A, which increases vascular permeability Anaphylatoxins C3A, C5A, which make phagocytic cells easily permeable to the blood vessel wall Chemokines C3A, C5A, C5B67 make phagocytic cells concentrate around antigens Immunomodulation: Complement cleavage products (C3B, C4B) ,.. after binding to pathogenic microorganisms

Biological function of complement.

1.Bacteriolytic and cytolytic effects.

The membrane attack complex formed by complement activation can lyse and destroy bacteria and cells, which is of great significance in the process of anti-infection immunity and immunopathology.

2.Regulates phagocytosis.

After the complement cleavage product C3B and C4B bind to granular antigens or immune complexes such as bacteria through the N-terminal unstable binding site, and then bind to phagocytic cells with corresponding complement receptors on the surface through the C-terminal stable binding site, the resulting phagocytosis is called complement opsonoptic phagocytosis.

3.Immunoadhesion.

C3B C4b binds to granular antigens or immune complexes such as bacteria, and then binds to red blood cells or platelets with corresponding complement receptors on the surface to form macromolecular complexes, which is the immune adhesion of complement. The macromolecular polymers formed by immune adhesion are easily engulfed and cleared, which is of great significance in the process of anti-infection immunity and clearance of immune complexes.

4.Inflammatory mediator action.

1) C2A has a kinin-like effect, which can dilate blood vessels, increase permeability, and cause inflammatory exudation and edema.

2) C3A, C4A and C5A have the effect of anaphylatoxin, which can degranulate mast cells and basophils, release vasoactive substances such as histamine, and cause symptoms such as vasodilation, enhanced permeability, smooth muscle contraction and bronchospasm.

3) C3A and C5A have chemotaxis, which can attract neutrophils and monocytic phagocytes to aggregate at the site of inflammatory lesions, exert phagocytosis, and release inflammatory mediators to cause or enhance inflammatory responses.