## Mediators of Acute Inflammation — Mechanism and Effects **Key Point:** PGE2 is a pro-inflammatory mediator that causes vasodilation and increases vascular permeability — it does NOT cause vasoconstriction or limit inflammation. This is the incorrect statement. ### Correct Mediators and Their Actions | Mediator | Source | Primary Action | Effect | |----------|--------|-----------------|--------| | Histamine | Mast cells, basophils | H1/H2 receptor activation | Vasodilation, ↑ permeability, pain | | Bradykinin | Kinin cascade (HMWK) | B2 receptor activation | Vasodilation, pain, smooth muscle contraction | | C5a | Complement activation | G-protein coupled receptor | Chemotaxis, degranulation, vasodilation | | PGE2 | COX pathway (arachidonic acid) | EP receptors | **Vasodilation, ↑ permeability, potentiates pain** | | Leukotrienes (LTC4, LTD4) | 5-lipoxygenase pathway | CysLT receptors | Potent vasodilation, ↑ permeability, chemotaxis | **High-Yield:** PGE2 and other prostaglandins (PGD2, PGI2) are pro-inflammatory — they amplify the inflammatory response, not suppress it. NSAIDs work by inhibiting COX enzymes, thereby reducing PG synthesis and inflammation. **Clinical Pearl:** The distinction between vasodilators (histamine, bradykinin, PGE2, leukotrienes) and vasoconstrictors (norepinephrine, angiotensin II) is clinically important. Acute inflammation is characterized by net vasodilation and increased permeability. ### Why Option 3 Is Wrong PGE2 causes: - Vasodilation (not vasoconstriction) - Increased vascular permeability (not decreased) - Potentiation of pain (synergizes with bradykinin) - Pro-inflammatory effects (not anti-inflammatory) **Warning:** Do not confuse PGE2 with catecholamines or vasopressin, which cause vasoconstriction. PGE2 is fundamentally a vasodilator and permeability-increasing agent.
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