Exudation of fluid from venules and capillaries is a key component of the acute inflammatory process. Several mechanisms of increased vascular permeability have been proposed, including formation of interendothelial gaps by contraction of endothelium. This contraction can be caused by mediators such as histamine and leukotrienes. The vessels then become more "leaky," and the fluid leaves the intravascular space to accumulate extravascularly, forming effusions in body cavities or edema within tissues. Arteriolar vasoconstriction is a transient response to injury that helps diminish blood loss. Platelets adhere to damaged endothelium and promote hemostasis. Lymphatic obstruction results in the accumulation of protein-rich lymph and lymphocytes, producing a chylous effusion within a body cavity. After neutrophils reach the site of tissue injury outside of the vascular space, they release lysosomal enzymes that promote liquefaction.