Abstract
At the height of development of acute aseptic inflammation of the subcutaneous cellular tissue the plasma kinin system in the general circulation becomes activated, as reflected in an increase of 1.5–2 times in kallikrein activity, an increase of 1.5–3 times in kininase activity, and a decrease of 25–26% in the kininogen level. The conditions are created for increased generalized formation and accumulation of free kinins, the mediators of the second phase of the disturbances of vascular permeability in inflammation.
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