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Figure 2 : 2 days after injury.
Tissue trauma stimulates the inflammatory response. Immediately after injury intense local vasoconstriction occurs, mediated by circulating catecholeamines and prostaglandins released by injured cells. This is followed by vasodilatation and increased capillary permeability resulting in local edema. This is mediated by histamine, kinins, prostaglandins, leukotrienes, and endothelial cell products.
Neutrophils are the first leukocytes to be found in wounded tissues. They phagocytose damaged tissue or bacteria. Neutrophils themselves are phagocytosed by macrophages. Pain in the area of injury is due to changes in pH due to break down of tissues and bacteria along with swelling and decreased tissue oxygenation due to disruption of blood vessels. Neutrophil count of the wound increases for 24-48 hrs and then declines unless wound contamination has occurred.
Monocytes transform into macrophages as they migrate from capillaries into extra vascular space. Macrocytes phagocytose bacteria and tissue debris and secrete enzymes (collagenase and elastase) responsible for breaking down damaged matrix. They also cytokines, P.G.s, oxygren free radicals and other regulators of wound healing.
Lymphocytes produce various factors like HB-EGF(Heparin binding epidermal growth factor), basic fibroblast growth factor and they are also involved in cellular and humoral immunity.
Initially for 24-48 hrs neutrophils dominate but 48-72hrs later they are outnumbered by macrophages which persist for few days. After 5-7 days fibroblasts are the predominant cell type.
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