Vascular Changes in Acute Inflammation
Bilal Asif Roll No. 28
Definition Inflammation is a protective
response intended to eliminate the initial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult.
Inflammation accomplishes its protective role by diluting, destroying, or otherwise neutralizing harmful agents (e.g., microbes and toxins).
Inflammtion
Acute: Transient and early response to injury that involves release of chemical mediators, causing specific vessel and leukocyte responses
Chronic: Inflammation of prolonged duration (weeks to years) that most often results from persistence of an injury-causing agent
Types
Rapid response to injurious stimuli carried out by leukocytes and plasma proteins at the site of injury, lasting for a few minutes to few days
Characterized by fluid and plasma protein exudation and neutrophilic leukocyte accumulation
Acute Inflammtion
Associated with vascular changes and cell recruitment
General features are1) swelling (tumor). 2) heat (calor), 3) redness (rubor)4) pain (dolor)5) loss of function
General Features
Three mechanisms are involved in Acute Inflammation
(Plasma Proteins, Vessels, Leukocytes)1. Changes in vascular flow and caliber
2. Structural changes in microvasculature
3. Immigration of Leukocytes
Mechanism Of Acute Inflammation
Inflammation
Response (depend upon severity and nature of stimulus)
Transient Vasoconstriction (Stress response)
Arteolar Vasodilation (histamine, NO) (to increase WBC to Inflammation)
Changes of Vascular Flow and Caliber
Increased Blood Flow Redness(Rubor), Warmth Increased Intravascular Hydrostatic PressureMovement of fluid in tissues
Transudate (Less Protein and Leukocytes)
More Increased Vascular Permeability
Exudate
(Increase Protein and Leukocytes)
Decreased Intravascular Osmotic Pressure Increase Osmotic Pressure of Interstitial Fluid
Outflow of water and ions in extravascular tissue
Edema
Stasis and Margination Increased Blood Flow
Protien rich fluid in Extravascular Tissue
Red blood cells become concentrated
(Increased blood viscosity/ Slow circulation)
Numerous dilated vessel with RBCs
Stasis
Leukocyes along vascular endothelium
Margination
Endothelial cell contraction cause intercellular gaps
histamine, bradykinin, leukotrienes and other chemical mediators
immediate transient response: is rapid contraction of Endothelial cell after binding of mediators to specific receptors, short-lived (15-30 minutes)
Immediate sustained response: slower and more prolonged retraction of endothelial cells, resulting from changes in the cytoskeleton
cytokines such as tumor necrosis factor (TNF) and interleukin-1 (IL-1).
Reaction may take 4 to 6 hours
Mechanism Of Increased Vascular Permeability
delayed prolonged leakage: after a delay of 2 to 12 hours, lasts for several hours or even days, and involves venules and capillaries
E.g. May occur due to mild to moderate thermal injury, certain bacterial toxins, and x- or ultraviolet irradiation
Leukocyte-mediated endothelial injury
Endothelial injury results in vascular leakage by causing endothelial cell necrosis and detachment
Due to leukocyte accumulation along the vessel wall
activated leukocytes release many toxic mediators
Increased transcytosis of proteins via an intracellular vesicular pathway via channels formed by fusion of intracellular vesicles
Occur by following four mechanisms which cause exudation
1) Retraction of endothelial lining by histamine, baradykinin, substance P causing the cells to shrink
2) Damage to endothelial lining (burns) cause exudation
3) Margination of leukocytes can act as injurious agent damaging endothelium
4) Transcytosis of proteins via an intracellular vesicular pathway via channels formed by fusion of intracellular vesicles
Structural changes in Microvasculature