GENERAL PATHOLOGY

Inflammation – Vascular Response

Transient vasoconstriction -> vasodilatation of arterioles -> hyperaemia ( ->rubor, calor)

Arteriolar dilatation occurs after vasoconstriction and results in an opening of the microvascular bed. Increased blood flow to the injured area is called hyperaemia and causes redness and heat – note also that there is an increase in the net pressure in capillaries and post capillary venules, leading to an outflow of fluid.

Direct injury to vessels (or venule endothelial cell contraction) causes alteration of vessel permeability, leading to leakage of fluid and plasma proteins:

• Endothelial cell contraction and separation of the endothelial junctions (in postcapillary venules) in response to mediators
• Increased hydrostatic filtration pressure enhances outward movement of fluid and facilitates the passage of larger protein molecules
• More sustained/serious injury leads to large gaps in endothelial junctions and these changes also affect capillaries (increasing the rate of extravascular fluid flux)
• Intravascular and extravascular osmotic pressure equalise, the hydrostatic pressure in the tissue increases (so fluid loss is dependent on net hydrostatic pressure)
• A protein-rich exudates accumulates extravascularly
• Due to tissue swelling, collagen fibres anchored in the tissue pull open terminal lymphatic channels – leading to increased lymph flow
• Lymphatic channels assist in draining the fluid and cellular exudates