Trauma-hemorrhagic shock-induced red blood cell damage leads to decreased microcirculatory blood flow

To test the hypothesis that trauma-hemorrhagic shock (T/HS)-induced changes in red blood cells (RBC) contribute to the reduction of blood flow in distant organs.

Laboratory study.

Academic medical center laboratory.

Specific pathogen-free male Sprague-Dawley rats weighing between 250 and 350 g.

Rats were transfused with trauma-sham shock (T/SS), or T/HS whole blood, or RBC-depleted blood (blood with the RBC removed and consisting of white blood cells and plasma).

Cardiac output and organ blood flow were measured by the radioactive microsphere technique. RBC tissue trapping, deformability, and RBC aggregation and adhesion were studied. Measurements of RBC adenosine triphosphate (ATP) and plasma fibrinogen were performed. Exchange transfusion with T/SS blood did not alter cardiac output or organ blood flow. However, cardiac output and blood flow in several organs were decreased when T/HS whole blood was used and RBCs were trapped in the organs that evidenced decreased blood flow. T/HS also increased RBC aggregation and adhesion, and decreased deformability. The ability of T/HS exchange transfusion to decrease microcirculatory blood flow did not appear to be due to plasma factors or non-RBC elements (i.e., white blood cell), because organ blood flow was not reduced after exchange transfusion with T/HS RBC-depleted blood. Likewise, neither decreased RBC ATP nor increased plasma fibrinogen explained the T/HS-induced changes that were observed. There was no change in fibrinogen levels during or after shock. Although there was a transient decrease in T/HS erythrocyte ATP levels during the early shock period, in contrast to RBC function, the ATP levels had returned to normal with resuscitation.

T/HS induces significant changes in RBC functions and the injection of T/HS, but not T/SS, RBC leads to decreased organ blood flow. These findings confirm the hypothesis that T/HS-induced RBC alterations will directly cause organ hypoperfusion and suggest that T/HS-induced RBC damage contributes to this process. Thus, T/HS-induced changes in RBC function may contribute to the development of shock-induced multiple organ failure.