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    Djumadi Achmad

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    BEBERAPA GOLONGAN Mediator :

    1. Amine vasoaktif : histamin, serotonin

    2. Protease plasma : komplemen, kinin,

    sistem pembekuan

    3. Metabolit asam arakhidonik : Prostaglandin,leukotrien

    4. Platelet Activating Factor (PAF)

    5. Sitokin : IL-1, IL-8, TNF

    6. Nitric oxide (NO)

    7. Enzim lisosomal dari lekosit

    8. Radikal bebas dari oksigen

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    Cell-derived mediators

    Diproduksi oleh :

    Platelet

    Mast cells / basophils Polymorphonuclear leukocytes

    Endothelial cells

    Monocytes / macrophages

    Injured tissue

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    Cell-derived mediators

    Pembentukannya :1. Preformed dan disimpan dalam

    granula sitoplasma (histamin,serotonin, enzim lisosomal)

    2. Berasal dari metabolisme asamarakhidonik (prostaglandin,leukotrien, tromboxan, platelet

    activating factor)3. Produk lain dari vascular regulator

    (NO)

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    Mast cell / basofil,

    Platelet

    Jejas fisik

    Rx imun : Ab-mast cell

    Komplemen : C3a, C5a

    Histamine-releasing protei

    dari lekosit

    Neuropeptide : substasi P

    Sitokin : IL-1, IL-8

    Vasodilatasi

    Hiperpermeabilitas

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    Platelet

    Kontak : kollagen,trombin, ADP, komp

    Ag-Ab

    PAF

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    Figure 2-16 Generation of arachidonic acid metabolites and their roles in inflammation. The molecular

    targets of action of some anti-inflammatory drugs are indicated by a red X. COX, cyclooxygenase; HETE,

    hydroxyeicosatetraenoic acid; HPETE, hydroperoxyeicosatetraenoic acid.

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    Metabolit Asam Arakhidonik

    Metabolit EfekTXA2, LTC4, LTD4, LTE4

    PGI2, PGE1, PGE2, PGD2

    LTC4, LTD4, LTE4

    LB4, HETE

    PGE2

    Vasokonstriksi

    Vasodilatasi

    Hiperpermeabilitas

    Khemotaktik

    Nyeri, demam

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    Mast cell / basofil, netrofil,

    monosit, endotel,

    Vasokonstriksi,

    spasme bronkhus

    Vasodilatasi

    Hiperpermeabilita

    Adhesi lekosit

    Khemotaksis

    Degranulasi

    Radikal bebas O-

    IgE mediated rx

    Membran fosfolipid

    PAF

    PLA2

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    Figure 2-18 Major effects of interleukin-1 (IL-1) and tumor necrosis factor (TNF) in inflammation.

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    Figure 2-19 Functions of nitric oxide (NO) in blood vessels and macrophages, produced by two

    NO synthase enzymes. NO causes vasodilation, and NO free radicals are toxic to microbialand mammalian cells. NOS, nitric oxide synthase.

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    Plasma-derived mediators

    1. Sistem komplemen

    2. Faktor Hageman (faktor XII)

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    Figure 2-14 The activation and functions of the complement system. Activation of complement by

    different pathways leads to cleavage of C3. The functions of the complement system are

    mediated by breakdown products of C3 and other complement proteins, and by the membrane

    attack complex (MAC).

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    Figure 2-15 Interrelationships between the four plasma mediator systems triggered by activation of factor

    XII (Hageman factor). Note that thrombin induces inflammation by binding to protease-activated receptors

    (principally PAR-1) on platelets, endothelium, smooth muscle cells, and other cells.

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    Sistem KININ

    Efek :

    Diinaktifkan oleh : Kininase

    1. Hiperpermeabilitas

    2. Kontraksi otot polos

    3. Vasodilatasi

    4. Nyeri