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