Experiments were conducted on models of immobilization stress and hemorrhagic shock in rabbits to study the changes in the ability of intravenously injected adrenaline (A) to induce blood neutrophilia due to the escape of parietal neutrophils into circulation. It is shown that immobilization stress, just like A infusion, leads to neutrophilia. In contrast, in hemorrhagic shock neutropenia develops and the response to A disappears. Such changes in massive blood loss are interpreted by the authors as transition of the marginal (physiological) adhesion of neutrophils in the vascular system to pathological adhesion characteristic of inflammatory reactions.
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