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.