Sunday, 10 March 2013

Acute Inflammation: Vascular Changes

Inflammation is the reaction of the body to an area of localised tissue injury. It is a complex progression of vascular and cellular changes that work together to dilute, destroy and isolate the injury and to repair the damaged tissue. There are five key signs of acute inflammation: pain, heat, redness, swelling, and loss of function.

Acute inflammation is short in duration and may last from a few minutes to a few days. It is characterised by marked vascular and moderate cellular responses. Chronic inflammation is much less vascular and more cellular and lasts from weeks to months.  

In this post we'll take an overall look at the process of acute inflammation before describing the vascular changes that are associated with this process. 

An Overview of Acute Inflammation

The process of acute inflammation can be described as a cycle. Firstly, tissue damage, which may be caused by infections, trauma, physical or chemical agents, foreign bodies, tissue necrosis and allergies, is induced. The body contains cells which sense this damage and cause a tissue response to occur through the release of soluble mediators. The tissue response works to remove the inducers of the tissue damage.

Vascular Changes of the Acute Inflammatory Response

The vascular changes in acute inflammation are important because they increase blood flow (which contains most of the reactive elements) to the affected area which allows the inflammatory response to occur. The sequence of events that occur are described below:
  1. Vasoconstriction: This is possibly due to adrenaline or other neurogenic control and the vasoconstriction is only fleeting.
  2. Active Hyperaemia: An axon reflex arc causes arterioles to dilate which causes capillary beds to open. This leads to the redness and heat which is seen in acute inflammation.
  3. Increased vessel permeability which causes fluid to move into the interstitial space. This increases blood viscosity and slows down blood outflow. The mechanisms by which the vascular permeability increases depends on the nature of the cause of the tissue damage. These mechanisms include:
    • The formation of gaps between the endothelial cells.
    • Direct endothelial injury
    • Leukocyte dependent injury which is caused by enzymes and mediators released by the leukocytes during transmigration (when leukocytes move across the endothelium).
    • Angiogenesis: new vessels may leak
    • Radiation Damage: eg sunburn (UV). 
  4. Increased hydrostatic pressure caused by increased inflow and decreased outflow causes increased fluid in the extracellular areas.
  5. White Cells marginate. This is caused by the slowing of blood which causes red cells to clump and flow in the central regions of blood flow while white cells move to the edges where they adhere to endothelial cells. 
    • Soluble mediators cause the endothelium to be activated which results in the upregulation of the selectins which are molecules on the surface of the endothelial cells
    • The white cells bind to the selectins. 
    • The integrin proteins are then activated and adhesion molecules assist the white cell to transmigrate through the endothelial cells.
  6. White Cells migrate to the site of tissue injury through chemotaxis. 


That's all for now, see you next time :)

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