Inflammation begins with characteristic vascular changes that help deliver immune cells and plasma proteins to the site of injury or infection.
These changes are dynamic and mediated by chemical factors released by injured tissues and immune cells.
Initial Vascular Response
- Transient Vasoconstriction
- Duration: Very short-lived (a few seconds).
- Purpose: Helps limit initial blood loss after injury.
- Mechanism: Reflex neurogenic response and endothelin release.
- Vasodilation
- Mechanism
- Mediators
- Histamine (from mast cells, basophils)
- Bradykinin (from the kinin system)
- Prostaglandins (PGE₂, PGI₂)
- Effects
- Increases local blood flow → erythema (redness) and heat.
- Marks the beginning of acute inflammation.
- Increased Vascular Permeability: Allows plasma proteins (e.g., fibrinogen, immunoglobulins) to escape into the interstitial space, forming exudate.
| Mechanism | Description | Key Mediators |
|---|---|---|
| Endothelial Cell Contraction | Causes the formation of intercellular gaps, mainly in postcapillary venules | Histamine, Bradykinin, Leukotrienes (LTC₄, LTD₄, LTE₄) |
| Direct Endothelial Injury | Necrosis/detachment of endothelial cells after burns or infections | Bacterial toxins, ROS, and physical injury |
| Leukocyte-Dependent Injury | Activated neutrophils release toxic oxygen species and proteases, damaging the endothelium | Neutrophil enzymes, ROS |
| Increased Transcytosis | Transport of fluids/proteins across the endothelium | VEGF (Vascular Endothelial Growth Factor) |
Outcome: Plasma leakage → tissue swelling (edema).
Hemodynamic Consequences
- Early phase Vasodilation → increased flow Redness (rubor), warmth (calor).
- Later phase ↑ : Viscosity due to fluid loss, Stasis (sluggish flow).
- Stasis: Blood cells move closer to the endothelium. Neutrophil margination and emigration begin.
Key Points to Remember
✅ Vasodilation → increased blood flow (histamine, prostaglandins)
✅ Increased permeability → endothelial contraction or injury (histamine, bradykinin, leukotrienes)
✅ Stasis → slows flow, promoting neutrophil margination
✅ Histamine acts in both vasodilation and increased permeability
✅ Bradykinin causes pain, vasodilation, and permeability increase
Learning Objective
By the end of this topic, you should be able to:
Describe the sequence of hemodynamic changes during acute inflammation, identify the key mediators involved, and explain how these vascular events facilitate leukocyte migration to the site of injury.
