This investigation was supported by the following grants: NIH R01 HL52684, R01 HL064395, and R01 HL062318 and ARMY W81XWH-11-2-0012.
Microhemodynamic aberrations created by transfusion of stored blood
Article first published online: 31 JUL 2013
© 2013 American Association of Blood Banks
Volume 54, Issue 4, pages 1015–1027, April 2014
How to Cite
Yalcin, O., Ortiz, D., Tsai, A. G., Johnson, P. C. and Cabrales, P. (2014), Microhemodynamic aberrations created by transfusion of stored blood. Transfusion, 54: 1015–1027. doi: 10.1111/trf.12361
- Issue published online: 11 APR 2014
- Article first published online: 31 JUL 2013
- Manuscript Accepted: 20 JUN 2013
- Manuscript Revised: 14 JUN 2013
- Manuscript Received: 22 APR 2013
- NIH. Grant Numbers: R01 HL52684, R01 HL064395, R01 HL062318
- ARMY. Grant Number: W81XWH-11-2-0012
Human red blood cells (RBCs) can be stored for up to 42 days under controlled conditions. Physical and chemical changes occur during RBC storage, altering their function. This study links stored cell mechanical changes with hemodynamic functional alterations upon transfusion.
Study Design and Methods
Mechanical properties of fresh and stored RBCs were evaluated in vitro. Their transfusion effects were evaluated in vivo using intravital microscopy of the rat's cremaster muscle preparation. Rats were hemodiluted to 30% hematocrit, to mimic an anemic state before transfusion, and then exchange-transfused with fresh or stored cells.
In vitro studies on rheology and oxygen affinity of stored cells confirmed previously published results. Storage was found to modify static and dynamic RBC mechanic behavior. After transfusion, systemic hemodynamics were similar for fresh and stored cells; however, microvascular hemodynamics were drastically affected by stored cells. Stored cells reduced blood flow and oxygen delivery. Additionally, the presence of stored cells in circulation affected cell-to-cell and cell-to-wall interactions and affected cell hydrodynamics. Stored cells disrupted the RBC cell-free layer and wall shear stress signals.
The reduced cell deformability due to RBC “storage lesions” caused pathologic changes in microvascular hemodynamics, endothelial cell mechanotransduction, and RBC dynamics. Thus, the mechanical changes of blood-banked cells can limit transfusion ability to achieve its intended goal.