Thermally Induced Erythrocyte Aggregation by Surface Nanobubble Coalescence

Erythrocyte aggregation is a reversible phenomenon, of which the mechanism is unknown. Pathological conditions, such as thermal burn injury and the presence of plasma proteins are associated with an increase of erythrocyte aggregation, particularly in the temperature range of 42°C to 45°C. Aggregation contributes to two‐phase flow, increasing the throughput of red blood cells. Excessive aggregation occludes vessels, inhibiting blood flow to tissues downstream. Reduced perfusion leads to hypoxia and ischemia in the region of thermal injury, ultimately resulting in thermal burn injury progression. During low Reynolds flow and stasis, fluid shear is less likely to monodisperse the red blood cells. Following thermal injury, aggregation happens within seconds. Aggregates remaining in the presence of fibrin for a four hour period will progress to clots. While the mechanism for aggregation is unknown, several models have been proposed, including the bridging model and depletion layer model; however, neither account for all possible biophysical phenomena. Here we propose a model in which nanobubbles on neighboring red blood cell surfaces have potential to coalesce, effectively increasing red cell aggregation. We hypothesize that during the onset of thermal injury, nanobubbles are formed by rapid blood‐gas dissolution furthered by simultaneous oxy‐hemoglobin dissociation. Nanobubble dynamics are a function of gas concentration, surface tension, and geometric properties of blood constituents. Using MATLAB (MathWorks), a mathematical model of gas content and bubble dynamics was constructed to predict the likelihood of nanobubble formation, coalescence, and contribution to aggregation. The results of the model predict temperature dependent erythrocyte aggregation only at pH, and oxygen partial pressures similar to that of venous blood.