Hemolysis Products Impair Nitric Oxide Function on Infusion

Rat study demonstrates vasoconstriction after infusion of plasma from stored red blood cell units

MONDAY, July 25 (HealthDay News) -- The products of hemolysis, which accumulate in blood stored under standard conditions, interact with nitric oxide (NO) on infusion and impair its vascular function, according to an experimental study published online July 11 in Circulation.

Chenell Donadee, M.D., from the University of Pittsburgh, and colleagues investigated the association between the products of red blood cell hemolysis, which form during blood storage, and impaired NO function. Nine blood units obtained from the Central Bank in Pittsburgh were nonleukoreduced and preserved under standard conditions and compared with leukoreduced units for the analysis of free hemoglobin and NO consumption. Samples were collected weekly, starting at four days, over a period of six weeks. In vivo studies using a rat model were also performed.

The investigators found that human red blood cells stored under standard blood bank conditions accumulate cell-free and microparticle-encapsulated hemoglobin, which on infusion reacts with and scavenges NO at a rate approximately 1,000 times faster than intact erythrocytes. In the in vivo studies, even low concentrations of hemoglobin (below 10 µmol/L) caused vasoconstriction in contrast to controlled infusions of methemoglobin and cyanomethemoglobin, which do not interact with NO, and resulted in reduced vasoconstrictor effects in the rat models. Plasma from stored human red blood cell units infused into rat circulation resulted in significant vasoconstriction.

"Even low levels of cell-free plasma hemoglobin are sufficient to inhibit endothelial NO signaling and induce vasoconstriction and hypertension," the authors write.

Two of the study authors are co-authors on patent applications relating to hemolysis treatment.

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