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An explanation of the mechanism of ultrasonic echogenicity in flowing blood is proposed based upon an in vitro study that indicates a causal relation between red cell aggregation and these echoes. Echogenicity was measured in vitro at 37 degrees, 24 degrees, and 0 degree C as blood flow shear rates were varied. Echogenicity increased at higher temperatures and lower shear rates. The directions of changes in blood echogenicity exactly paralleled previously known changes in red cell aggregation resulting from changes in temperature. The authors consider this to be further evidence that red cell aggregation is an important cause of low-intensity echoes observed in clinical ultrasonography of the heart and circulation.

The role of red cell aggregation as a cause of ultrasonic echogenicity in flowing blood was evaluated by in vitro experiments using fresh human blood. Blood was circulated in tubes of varying diameter (12 mm to 6 mm). In all experiments, echogenicity increased as blood approached static conditions. Echogenicity was greater in tubes with a larger diameter over the same range of blood velocity. However, echogenicity in tubes of various diameters was the same when evaluated in terms of shear rate. Thus, shear rate and not velocity is the flow condition that determines echogenicity. Since shear rate determines the degree of red cell aggregation, while other conditions affecting red cell aggregation (hematocrit, erythrocyte membrane conditions, and plasma macromolecules) are held constant, we conclude that these results provide additional evidence that red cell aggregation is a cause of echogenicity in flowing blood. Furthermore, a red cell aggregation mechanism for blood-flow echogenicity would explain the increased prominence of internal echoes in lower shear rate venous blood flow compared with those of higher shear rate arterial blood flow.

High-resolution ultrasonic imaging of circulating blood was used to study the relation between red cell aggregation and blood clotting in vitro. A reversible increase in echogenicity produced by red cell aggregation occurred in moving heparinized blood as shear rate was decreased. We induced clotting of the heparinized blood by administration of protamine. At both low (1.6 sec-1) and moderate (22.6 sec-1) mean shear rates, transient homogenous increased echogenicity indicative of red cell aggregation preceded blood clotting. In separate experiments, we established that protamine can cause increased echogenicity due to red cell aggregation which can be reversed by adding heparin to circulating suspended red cells in the absence of clotting factors. Presumably, these effects of protamine and heparin are due to electrostatic bonding involving red cell surfaces. We conclude from these studies that red cell aggregation precedes clotting of heparinized blood by protamine at low and moderate shear rates.