State-of-the-art conception of stress is represented as an interrelation between stress, tissue hypoxia and adaptation. Under the influence of stressors the cell metabolism changes with producing of chemical substances capable pathologically to get bound with cell receptors. These substances change in cells optimal energy transformation (biochemical stage) and disturb cell functions (pharmacological stage). Biochemical and pharmacological stages of stress in uncellulates and in human cells are homotypic. The clinical stage of stress is typical only for humans and animals. Dysfunction of plane muscles (PM) myocytes leads to local microcirculation disturbances, transitory hypoxia and partial disorder in affected organ function. Local microcirculation disturbances are accompanied by serotonin release from damaged platelets, which leads to complete functional recovery of PM myocytes, microcirculation and affected organ function, or to formation of local "mute" focuses of tissue necrosis--the adaptation is effective. Insufficient serotonin release from damaged platelets leads to extension of hypoxia focus, lesion, tissue necrosis. The stress loses its nonspecificity and turns into infarction of myocard, brain etc., with specific clinical course--the adaptation is not effective.