All of the following are false regarding vascular leakage in acute inflammation, except:
Several mechanisms are responsible for the increased permeability of postcapillary venules, a hallmark of acute inflammation. Chemical mediators such as histamine, bradykinin, leukotrienes, elicit endothelial cell contraction which is the immediate transient response. This results in increased interendothelial spaces - the most common mechanism of vascular leakage. In most instances, leakage stas immediately after injury and is sustained for several hours until the damaged vessels are thrombosed or repaired. Increased transpo of fluids and proteins through the endothelial cell, called transcytosis, also contributes to vascular leakage.
Chemical mediators such as histamine play a role in delayed vascular leakage.
Hallmark of acute inflammation is an increased permeability in the post-capillary venules.
Transcytosis is not a contributing factor to vascular leakage.
In most cases, vascular leakage stas several hours after injury.
Basic Concepts and Vascular changes of Acute Inflammation