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The local inflammatory changes sometimes cause erythrocyte hemolysis, platelet aggregation, and adhesion to the ablated epithelium cells of capillary vessels [ 7 ]. They are responsible not only for the micro-blood clot formation but also for the occurrence of the DIC [ 413 ]. These processes are dynamic and rapid. The rise of the permeability of vessels causes the swelling of the connective tissue structures, e. The fibroblasts are induced to divide and the blood corpuscles such as collagen and, as a consequence—elastic fibers—are produced. They form the demarcation line of the inflammation and neutralize the toxic effect of inflammatory products [ 415 ].

The slow blood flow in the inflammatory focus causes an increase of the vascular resistance and makes the diapedesis of leukocytes easier e. Consequently, the inflammatory mediators are absorbed on their cell membranes and the increase of the permeability of blood vessels leads to serum protein migration through this barrier e. After the intravascular coagulation, fibrinogen forms a local network where cell elements fall [ 18 ]. The intracellular fluids flow across the lymphatic vessels to regional lymph nodes in the inflammatory focuses. Swelling and pain are the most characteristic features [ 1920 ]. A lot of neutrophils, eosinophiles, and thrombocytes appear in the fourth and fifth hour of the inflammatory reaction [ 192122 ].

The leukocytes produce free radicals and superoxide ions [ 20232425 ], and granulocytes activate the release of prostaglandins e. Migrating granulocytes in the inflammatory focus cause the local necrobiotic changes, and they damage the intrafollicular and intralobular septum in the lungs because of the presence of elastase in neutrophils [ 46212228 ]. Currently, no data has shown dioxin interaction on the basic morphologic blood parameters including the erythrocyte and leukocyte system, which is used for inflammation monitoring. Probably, immunosuppressive dioxin action can significantly influence blood parameters, mainly by generation of free radicals and induction of pro-inflammatory cytokines.

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