Vascular Events
In addition to the vascular changes associated with the bleeding, there
are also marked changes in the state of the intact vessels. There are changes
in the caliber of the blood vessels, changes in the vessel wall and in the flow
of blood through the vessels. Vasodilation follows an initial but brief
vasoconstruction and persists for the duration of the inflammatory response.
Flow increases through the main channels and additionally previously dormant
capillaries are opened to increase the volume through the capillary bed. The
cause of this dilation is primarily by chemical means (histamine,
prostaglandins and complement cascade components C3 and C5) while the axon
reflex and autonomic system exert additional influences. There is an initial
increase in velocity of the blood followed by prolonged slowing of the stream.
The white cells marginate, platelets adhere to the vessel walls and the
endothelial cells swell. In addition to the vasodilation response, there is an
increase in the vasopermeability of the local vessels (also mediated by
numerous of the chemical mediators), and thus the combination of the
vasodilation and vasopermeability response is that there is an increased flow
through vessels which are more “leaky”, resulting in an increased exudate
production.
The
flow and pressure changes in the vessels allow fluid and the smaller solutes to
pass into the tissue spaces. This can occur both at the arterial and venous
ends of the capillary network as the increased hydrostatic pressure is
sufficient to overcome the osmotic pressure of the plasma proteins. The vessels
show a marked increase in permeability to plasma proteins. There are several
phases to the permeability changes but essentially, there is a separation of
the endothelial cells, particularly of the venules, and an increased escape of
protein rich plasma to the interstitial tissue spaces. The chemical mediators
responsible for the permeability changes include histamine, serotonin (5-HT),
bradykinin and leukotreines together with a potentiating effect from the
prostaglandins.
The
effect of the exudate is to dilute any irritant substances in the damaged area
and due to the high fibrinogen content of the fluid. A fibrin clot can also
form, providing an initial union between the surrounding intact tissues and a
meshwork which can trap foreign particles and debris. The meshwork also serves
as an aid to phagocytic activity. Mast cells in the damaged region release
hyaluronic acid and other proteoglycans which bind with the exudate fluid and
create a gel which limits local fluid flow, and further traps various particles
and debris.
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