Decompensated Liver Cirrhosis Impairs the Deformability of Erythrocytes and Their Ability to Pass Through Microchannels

Red blood cells (RBC, erythrocytes) are the main cell population that ensures tissue oxygenation and forms the ordered movement of all blood cells through the vessels. Disturbances in the physiological deformability of red blood cells aggravate the degree of anemia in two ways: aberrant red blood cells are rapidly eliminated by sequestration and destruction in the spleen and liver; and second, poorly deformable red blood cells have a reduced potential for gas exchange in the capillaries due to a decrease in the membrane contact area. Regardless of the etiology of hepatosis, liver cirrhosis (LC) develops persistent anemia, but disorders of erythrocyte deformability in patients with decompensated liver cirrhosis have been poorly studied. Using laser diffraction, flow cytometry, and microfluidic analysis, we showed that erythrocytes of LC patients develop disorders of deformability caused by the stress type of erythropoiesis (release of immature reticulocytes into circulation, an increase in the proportion of phosphatidylserine-presenting erythrocytes, a decrease in the activity of cytosolic esterases. In LC, erythrocytes have a pronounced rigidity to hypoosmotic load: induced hemolysis is incomplete, its speed is reduced, which indicates a decrease in the deformability of erythrocytes. Deformability disorders affected the ability of erythrocytes to pass through microchannels - the transit velocity was decreased, a high percentage of occlusions was observed, i.e., signs of microrheology disorders were identified. A connection was established between the disorders of erythrocyte microrheology depending on the degree of LC progression.