Figure 1.

Tissue stress and general pathological processes (from Gusev E. et al., 2021). Note: The ratio of intensity to prevalence of damaging factors initiating a “response” in the form of tissue proinflammatory stress—a common pathogenetic underpinning of all pathological processes—can be used to distinguish three “big” general pathological processes (classical inflammation, SI, and ChLGI). The “inflammatory microcirculation”—a reaction of microvessels that causes a clinically significant exudative reaction and enormous migration of leukocytes into a damaged area with the emergence of an inflammation focus—is the key differentiating phenomenon for their distinction. (1) The presence of an inflammation focus (upper-left corner in Figure 1) and, in some cases, systemic manifestations of tissue stress at a subthreshold level for “inflammatory microcirculation” characterize classical inflammation. These systemic reactions are, for the most part, protective and aimed at providing resource support for the inflammation’s focal point (immune response, acute-phase response of the liver, forced leukocytopoesis, neuroendocrine stress, and mobilization of metabolic reserves). (2) Systemic inflammation (SI) is characterized by shockogenic systemic “inflammatory microcirculation” and presence of a transitional “gray” zone, in which it is impossible to prove or refute the presence of SI in situations of “pushing” variant development (upper right-hand corner of the figure). (3) Para-inflammation (low-intensity inflammation) can be local (see the figure in the lower left-hand corner of figure) or can spread throughout the body (see ChLGI) (lower right-hand corner of figure) Signs of endotheliosis and, in certain circumstances, latent microcirculatory disorders may be encountered within these types of tissue proinflammatory stress.