Vasodilation is induced by the action of several mediators, notably histamine, on vascular smooth muscle. It is one of the earliest manifestations of acute inflammation, and may be preceded by transient vasoconstriction. Vasodilation first involves the arterioles and then leads to the opening of new capillary beds in the area. The result is increased blood flow, which is the cause of heat and redness (erythema) at the site of inflammation.
Vasodilation is quickly followed by increased permeability of the microvasculature, with the outpouring of protein-rich fluid (an exudate) into the extravascular tissues.
The loss of fluid and increased vessel diameter lead to slower blood flow, concentration of red cells in small http://ebooksmedicine.net
A. NORMAL
B. EXUDATE (high protein content, and may contain some white and red cells)
C. TRANSUDATE (low protein content, few cells)
Increased hydrostatic pressure (venous outflow obstruction, [e.g., congestive heart failure])
Decreased colloid osmotic pressure (decreased protein synthesis [e.g., liver disease]; increased protein loss [e.g., kidney disease]; protein malnutrition [e.g., kwashiokor])
Fig. 3.2 Formation of exudates and transudates. (A) Normal hydrostatic pressure (blue arrow) is about 32 mm Hg at the arterial end of a capillary bed and 12 mm Hg at the venous end; the mean colloid osmotic pressure of tissues is approximately 25 mm Hg (green arrow), which is equal to the mean capillary pressure. Therefore, the net flow of fluid across the vascular bed is almost nil. (B) An exudate is formed in inflammation because vascular permeability increases as a result of retraction of endothelial cells, creating spaces through which fluid and proteins can pass. (C) A transudate is formed when fluid leaks out because of increased hydrostatic pressure or decreased osmotic pressure.
vessels, and increased viscosity of the blood. These changes result in stasis of blood flow, engorgement of small vessels jammed with slowly moving red cells, seen histologically as vascular congestion and externally as localized redness (erythema) of the involved tissue.
• As stasis develops, blood leukocytes, principally neutrophils, accumulate along the vascular endothelium. At the same time endothelial cells are activated by mediators produced at sites of infection and tissue damage, and express increased levels of adhesion molecules. Leukocytes then adhere to the endothelium, and soon afterward they migrate through the vascular wall into the interstitial tissue, in a sequence that is described later.
Several mechanisms are responsible for increased vascular permeability in acute inflammation (
Fig. 3.3 ), which include:
Retraction of endothelial cells resulting in opening of inter-endothelial spaces is the most common mechanism of vascular leakage. It is elicited by histamine, bradykinin, leukotrienes, and other chemical mediators. It occurs rapidly after exposure to the mediator (within 15 to 30 minutes) and is usually short-lived; hence, it is referred to as the immediate transient response, to distinguish it from the delayed prolonged response that follows endothelial injury, described next. The main sites for this rapid increase in vascular permeability are postcapillary venules.
Endothelial injury, resulting in endothelial cell necrosis and detachment. Direct damage to the endothelium is encountered in severe injuries, for example, in burns, or is induced by the actions of microbes and microbial toxins that target endothelial cells. Neutrophils that adhere to the endothelium during inflammation may also injure the endothelial cells and thus amplify the reaction. In most instances leakage starts immediately after injury and is sustained for several hours until the damaged vessels are thrombosed or repaired.