” Increased vascular permeability is the hallmark of acute inflammation.”
CAUSES OF VASCULAR PERMEABILITY :-
- It is caused by the separation of the endothelial cells resulting in the movement of fluids, cells and proteins out of the blood vessels collectively called as exudate.
- The exudate is a protein rich fluid which is responsible foe the swelling (tumor) associated with an injury.
- It is maxima,y seen in venules.
1.] In and around the inflamed tissue, their is accumulation of edema fluid in the interstitial compartment which comes from the blood plasma
2.] In the initial stage the escape of the fluid is due to the vasodilation and consequent elevation in hydrostatic pressure.
3.] The appearance of inflammatory edema due to increased vascular permeability of microvascular bed is explained on the basis of Starling’s hypothesis.
4.] According to Starling’s hypothesis the fluid balance is maintained by two opposing sets of forces :-
- Forces that causes outward movement of fluid from microcirculation : These are intravascular hydrostatic pressure and colloid osmotic pressure of interstitial fluid.
- Forces that cause inward movement of interstitial fluid in circulation : There are intravascular colloid osmotic pressure and hydrostatic pressure of interstitial fluid.
PATTERNS OF INCREASED VASCULAR PERMEABILITY :-
1.] Increased vascular permeability in acute inflammation by which normally non – permeable endothelial layer of microvascular become leaky can have following patterns and mechanism :
- Contraction of endothelial cells.
- Contraction or mild endothelial damage.
- Direct injury to endothelial cells.
- Leukocytes mediated endothelial injury.
- Leakiness in neurovascularisation.
Above figure is taken for Educational purpose only from Saad Hussai Et al 2015 (DOI: 10.13140/2.1.1526.0968)
DISORDERS OF VASCULAR PERMEABILITY :-
The endothelial barrier maintains vascular and tissue homeostasis and modulates many physiological processes, such as angiogenesis.
Vascular barrier integrity can be disrupted by a variety of soluble permeability factors, and changes in barrier function can exacerbate tissue damage during disease progression. Understanding endothelial barrier function is critical for vascular homeostasis.
Many of the signaling pathways promoting vascular permeability can also be triggered during disease, resulting in prolonged or uncontrolled vascular leak. It is believed that recovery of the normal vasculature requires diminishing this hyperpermeable state. Although the molecular mechanisms governing vascular leak have been studied over the last few decades, recent advances have identified new therapeutic targets that have begun to show preclinical and clinical promise. These approaches have been successfully applied to an increasing number of disease conditions.
MULTIPLE CHOICE QUESTIONS [MCQs] :-
1.] Vasoconstriction in acute inflammation is shown by ?
2.] Increased permeability in acute inflammation is due to ?
b. IL – 2
3.] All the following vascular changes are observed in acute inflammation except ?
b. Status of blood
c. Increased vascular permeability
d. Decreased hydrostatic pressure
4.] Which of the following is the most characteristic feature of acute inflammation ?
a. Vasodilation and increased vascular permeability
b. Margination of leukocytes
d. Vascular stasis
5.] The hallmark of acute inflammation is ?
a. Increased blood flow
b. Increased vascular permeability
c. Vascular stasis
d. All of the above
6.] The role of histamine in acute inflammatory response include ?
a. Platelet release and aggregation
b. Increased vascular permeability of the venules
c. Membrane lysis
d. None of the above
7.] The complex process of leukocyte movement through the blood vessel are all except ?
a. More protein
8.] All the following are signs of inflammation except ?
d. Absence of functional loss
9.] In acute inflammation the tissue response consist of all except .
c. Neutrophilic response
d. Granuloma formation
10.] Brandykinin causes ?
a. Pain at the site of inflammation
d. None of the above
1.] (b) Arterioles
2.] (a) Histamine
3.] (d) Decreased hydrostatic pressure
4.] (a) Vasodilation and increased vascular permeability
59] (b) Increased vascular permeability
6.] (b) Increased vascular permeability of the venules
7.] (d) Phagocytosis
8.] (d) Absence of functional loss
9.] (d) Granulaoma formation
10.] (a) Pain at the site of inflammation
1.] Textbook Of Pathology By Harsh Mohan; 7th edition; Page no. 117 – 119.
2.] Robbin’s Basic Pathology; 5th edition; Page no. 54 – 56.