1.
Chemical response
Chemical response
2.
Vascular response
Vascular response
3.
Cellular response
Cellular response
Chemical Response
One of the best-known
chemical responses to stimuli is the release of histamine,
which triggers vasodilation and increases vascular permeability. Stored in
granules of circulating basophils and mast cells, histamine is released immediately
when these cells are injured. Other substances involved in increasing vascular
permeability are lysosomal compounds, which are released from neutrophils.
chemical responses to stimuli is the release of histamine,
which triggers vasodilation and increases vascular permeability. Stored in
granules of circulating basophils and mast cells, histamine is released immediately
when these cells are injured. Other substances involved in increasing vascular
permeability are lysosomal compounds, which are released from neutrophils.
Vascular Response
When
tissue is first injured, the small blood vessels in the damaged area constrict
momentarily, a process called vasoconstriction. Following this transient event,
which is believed to be of little importance to the inflammatory response, the
blood vessels dilate (vasodilation), increasing blood
flow into the area. Vasodilation may last from 15 minutes to several hours.
tissue is first injured, the small blood vessels in the damaged area constrict
momentarily, a process called vasoconstriction. Following this transient event,
which is believed to be of little importance to the inflammatory response, the
blood vessels dilate (vasodilation), increasing blood
flow into the area. Vasodilation may last from 15 minutes to several hours.
Next,
the walls of the blood vessels, which normally allow only water and salts to
pass through easily, become more permeable. Protein-rich fluid, called exudate,
is now able to exit into the tissues. Substances in the exudate include
clotting factors, which help prevent the spread of infectious agents throughout
the body. Other proteins include antibodies that help destroy invading
microorganisms.
the walls of the blood vessels, which normally allow only water and salts to
pass through easily, become more permeable. Protein-rich fluid, called exudate,
is now able to exit into the tissues. Substances in the exudate include
clotting factors, which help prevent the spread of infectious agents throughout
the body. Other proteins include antibodies that help destroy invading
microorganisms.
As
fluid and other substances leak out of the blood vessels, blood flow becomes
more sluggish and white blood cells begin to fall out of
the axial stream in the centre of the vessel to flow nearer the vessel wall.
The white blood cells then adhere to the blood vessel wall, the first step in
their emigration into the extravascular space of the tissue
fluid and other substances leak out of the blood vessels, blood flow becomes
more sluggish and white blood cells begin to fall out of
the axial stream in the centre of the vessel to flow nearer the vessel wall.
The white blood cells then adhere to the blood vessel wall, the first step in
their emigration into the extravascular space of the tissue
Cellular Response
The
most important feature of inflammation is the accumulation of white blood cells
at the site of injury. Most of these cells are phagocytes,
certain “cell-eating” leukocytes that ingest bacteria and other foreign
particles and also clean up cellular debris caused by the injury. The main
phagocytes involved in acute inflammation are the neutrophils,
a type of white blood cell that contains granules of cell-destroying enzymes
and proteins. When tissue damage is slight, an adequate supply of these cells
can be obtained from those already circulating in the blood. But, when damage
is extensive, stores of neutrophils—some in immature form—are released from the
bone marrow, where they are generated.
most important feature of inflammation is the accumulation of white blood cells
at the site of injury. Most of these cells are phagocytes,
certain “cell-eating” leukocytes that ingest bacteria and other foreign
particles and also clean up cellular debris caused by the injury. The main
phagocytes involved in acute inflammation are the neutrophils,
a type of white blood cell that contains granules of cell-destroying enzymes
and proteins. When tissue damage is slight, an adequate supply of these cells
can be obtained from those already circulating in the blood. But, when damage
is extensive, stores of neutrophils—some in immature form—are released from the
bone marrow, where they are generated.
To perform their tasks, not only must neutrophils
exit through the blood vessel wall but they must actively move from the blood
vessel toward the area of tissue damage. This movement is made possible by
chemical substances that diffuse from the area of tissue damage and create a
concentration gradient followed by the neutrophils. The substances that create
the gradient are called chemotactic factors, and the one-way migration of cells
along the gradient is called chemotaxis.
exit through the blood vessel wall but they must actively move from the blood
vessel toward the area of tissue damage. This movement is made possible by
chemical substances that diffuse from the area of tissue damage and create a
concentration gradient followed by the neutrophils. The substances that create
the gradient are called chemotactic factors, and the one-way migration of cells
along the gradient is called chemotaxis.
Large numbers of neutrophils reach the site of
injury first, sometimes within an hour after injury or infection. After the
neutrophils, often 24 to 28 hours after inflammation begins, there comes
another group of white blood cells, the monocytes, which eventually mature into
cell-eating macrophages. Macrophages usually become more prevalent at the site
of injury only after days or weeks and are a cellular hallmark of chronic
inflammation.
injury first, sometimes within an hour after injury or infection. After the
neutrophils, often 24 to 28 hours after inflammation begins, there comes
another group of white blood cells, the monocytes, which eventually mature into
cell-eating macrophages. Macrophages usually become more prevalent at the site
of injury only after days or weeks and are a cellular hallmark of chronic
inflammation.