Given that the two main components of resistance to pathogenic microorganisms, i.e., leukocytes and antibodies, are transported by the bloodstream, three alterations, namely, altered hemodynamics, increased vascular permeability, and leukocyte exudation, are evident in acute inflammation. The result is an accumulation of protein-rich exudate, fibrin and leukocytes in the extravascular space at the site of injury. This is the main feature of the pathohistology of acute inflammation. The maintenance of vascular permeability of the microcirculation depends primarily on the integrity of endothelial cells. During inflammation, the following mechanisms can cause an increase in vascular permeability. 1, endothelial cell contraction in histamine, bradykinin and other inflammatory mediators and endothelial cell receptor binding, can rapidly cause endothelial cell contraction, resulting in the formation of a gap between the endothelial cells of about 0.5 ~ 1.0 μm wide. Because of the short half-life of these inflammatory mediators of only 15-30 minutes, this response is called rapid-onset transient response. This reaction involves only the fine veins of 20-60 μm caliber, while the fine arteries and capillaries are not involved. Antihistamine drugs can inhibit this reaction. 2.Direct endothelial injury. Severe stimuli such as severe burns and pyogenic infections can directly cause endothelial cell damage, causing necrosis and detachment. Increased vascular permeability occurs rapidly and persists at high levels for hours to days until a thrombus forms within the damaged vessel, a process known as tachyphylactic sustained response. Microcirculatory vessels at all levels of fine arteries, capillaries, and fine veins can be involved. Mild to moderate thermal injury, X-ray and ultraviolet light injury, and direct endothelial cell damage caused by certain bacterial toxins occur later, often after 2 to 12 hours, but can last from a few hours to a few days and are called delayed-onset sustained reactions. This reaction only involves capillaries and small veins. 3.Leukocyte mediated endothelial injury. In the early stage of inflammation, leukocytes attach to the wall and adhere to endothelial cells, causing activation of leukocytes and release of active oxygen metabolites and protein hydrolases. The latter can cause endothelial cell damage or detachment and increase vascular permeability. 4, the high permeability of the new capillary wall in the repair process of the formation of the new capillary buds, the endothelial cell connections of the immature development of the endothelial cell connections, which can illustrate the healing inflammation in the fluid extravasation and edema.