Experiments studies which showed are carried out that stress hormones (a cortisol, adrenaline) can bind to erythrocyte membranes with high affinity, leading to rough structural changes. The last are accompanied by increase of microviscosity of membranes as in area a lipid-lipid, and protein-lipid of interactions. The nature of these changes is caused by simultaneous interaction of active groups of hormones (NH, OH and their waterproof rings) at the same time with a lipid and protein components of a membrane with formation of domains. Experiments with heart perfusion of rats showed that erythrocytes with the increased microviscosity of their membranes are incapable to move ahead on the capillary course that leads to sharp decrease in a coronary stream and fast cardiac arrest. The assumption is come out that this mechanism is shown and at a coronary syndrome X at the person.
