The wounding process involves damage to the microvasculature with a concurrent activation of several chemoattractant and growth factor pathways. Following wounding, inflammatory cells are attracted to the area of injury by products of the complement cascade and by-products released from degranulating platelets. The partial pressure of oxygen in wounds and flaps is inversely correlated with the risk for infection. Activated macrophages finction as phagocytes and also control granulation tissue formation by producing a variety of substances. The high metabolic rate of inflammatory cells in the hypoperfused wound space creates a unique microenvironment characterized by low pH, low dissolved oxygen concentration, low glucose, and high concentrations of carbon dioxide and lactate.
Oxygen diffuses from surrounding, functional capillary arcades.
However, it is rapidly consumed so that the gradient of oxygen across the wound margin is very steep. The oxygen tension in the region of a proximal arteriole is nearly 100 mmHg, but at distances of only 100 to 150 microns away from the capillary lumen, the oxygen tension has been found to be as low as 0 to 15 mmHg. The unusual characteristics present in the wound environment activate macrophages, which release potent growth factors as well as high concentrations of lactate. Fibroblasts respond to lactate and to macrophage-derived factors by multiplying and migrating, along with the macrophages, into the wound space. Restoration of the microvasculature occurs by endothelial buds, derived from venules, which are supported by the developing collagen scaffolding that is synthesized by fibroblasts.