LETTERS TO THE EDITOR
Stored red blood cells impair vascular function in vivo We have read with great interest the recent results of progressive impairments in nitric oxide (NO)–mediated vasodilation through stored red blood cells (RBCs).1 Because of their in vitro studies, Alexander and colleagues concluded that RBC-mediated vasoinhibitory mechanism did not work by NO scavenging. Although they recognize that their results do not specifically argue against vasoconstriction caused by cell-free hemoglobin (Hb), they arrive at the conclusion that the RBC-derived inhibitory activity appears much more potent than the vasoconstrictive activity of cell-free Hb. In view of these findings, the results of an in vivo study recently finished by our group may add valuable additional insight on the vasoinhibitory activity of stored RBCs. After transfusion of stored RBCs (older than 14 days) we found indications for enhanced scavenging of vasodilating nitric oxide by cell-free Hb. We conducted detailed hemodynamic and biochemical studies in 16 patients requiring transfusion of RBCs. The arterial function was studied noninvasively. In particular, we determined the pulse wave velocity as well as the aortic augmentation index as indicators of arterial stiffness. Patients (n = 8) who received stored RBCs showed a significantly increased aortic augmentation index (27.67% vs. 20.67%, p = 0.04) as well as an enhanced pulse wave velocity (13.46 m/sec vs. 11.45 m/sec, p = 0.004). Additionally, stored RBCs increased the nitrosylhemoglobin concentration (0.061 μmol/L vs. 0.018 μmol/L, p = 0.048) in transfusion recipients, possibly due to increased reaction between cell-free Hb (released because of agedepended RBC hemolysis) and nitric oxide. The described hemodynamic and biochemical alterations were absent in patients (n = 8) who received fresh RBCs (younger than 14 days). These data document that transfusion of aged RBCs has profound effects on arterial function in patients and show that the vasoconstrictive activity of free Hb may exceed what Alexander and colleagues assume in their studies. In addition to large clinical meta-analyses2,3 our results provide further evidence of the mechanism of deleterious transfusion outcomes in patients with stored RBCs.
© 2014 AABB
CONFLICT OF INTEREST The authors declare no conflicts of interest.
Mathias Forkmann, MD e-mail: [email protected] Marian Christoph, MD Karim Ibrahim, MD Marko Swoboda, PhD Steffen Kolschmann, MD Ruth H. Strasser, PhD Carsten Wunderlich, MD Department of Cardiology Medical Clinic University of Technology Dresden, Germany
REFERENCES 1. Alexander JT, El-Ali AM, Newman JL, et al. Red blood cells stored for increasing periods produce progressive impairments in nitric oxide-mediated vasodilation. Transfusion 2013;53:2619-28. 2. Wang D, Sun J, Solomon SB, et al. Transfusion of older stored blood and risk of death: a meta-analysis. Transfusion 2012;52:1184-95. 3. Tinmouth A, Fergusson D, Yee IC, et al. Clinical consequences of red cell storage in the critically ill. Transfusion 2006;46:2014-27.
Anti-A and anti-B titers in group O platelet units are reduced in PAS C versus conventional plasma units Platelets (PLTs) stored in additive solution (PAS) remove a substantial fraction of plasma and replace it with an isotonic buffered solution. PAS C are apheresis PLTs stored in PAS 3 buffer (InterSol, Fenwal, Inc., a Fresenius-Kabi company, Lake Zurich, IL). PAS 3 is the first AS available in the United States and stores apheresis PLTs collected with the Amicus separator (Fenwal, Inc.) in a solution containing 65% PAS/35% plasma. Theoretically, this process should remove 65% of the plasma proteins, including isohemagglutinins. Transfusion of PLT units with high isohemagglutinin titers can pose a risk of hemolysis if the unit crosses ABO type. This risk is greater when group O PLTs are released to non-O patients. Many blood banks titer all O units and Volume 54, January 2014 TRANSFUSION
255
Stored red blood cells impair vascular function in vivo We have read with great interest the recent results of progressive impairments in nitric oxide (NO)–mediated vasodilation through stored red blood cells (RBCs).1 Because of their in vitro studies, Alexander and colleagues concluded that RBC-mediated vasoinhibitory mechanism did not work by NO scavenging. Although they recognize that their results do not specifically argue against vasoconstriction caused by cell-free hemoglobin (Hb), they arrive at the conclusion that the RBC-derived inhibitory activity appears much more potent than the vasoconstrictive activity of cell-free Hb. In view of these findings, the results of an in vivo study recently finished by our group may add valuable additional insight on the vasoinhibitory activity of stored RBCs. After transfusion of stored RBCs (older than 14 days) we found indications for enhanced scavenging of vasodilating nitric oxide by cell-free Hb. We conducted detailed hemodynamic and biochemical studies in 16 patients requiring transfusion of RBCs. The arterial function was studied noninvasively. In particular, we determined the pulse wave velocity as well as the aortic augmentation index as indicators of arterial stiffness. Patients (n = 8) who received stored RBCs showed a significantly increased aortic augmentation index (27.67% vs. 20.67%, p = 0.04) as well as an enhanced pulse wave velocity (13.46 m/sec vs. 11.45 m/sec, p = 0.004). Additionally, stored RBCs increased the nitrosylhemoglobin concentration (0.061 μmol/L vs. 0.018 μmol/L, p = 0.048) in transfusion recipients, possibly due to increased reaction between cell-free Hb (released because of agedepended RBC hemolysis) and nitric oxide. The described hemodynamic and biochemical alterations were absent in patients (n = 8) who received fresh RBCs (younger than 14 days). These data document that transfusion of aged RBCs has profound effects on arterial function in patients and show that the vasoconstrictive activity of free Hb may exceed what Alexander and colleagues assume in their studies. In addition to large clinical meta-analyses2,3 our results provide further evidence of the mechanism of deleterious transfusion outcomes in patients with stored RBCs.
© 2014 AABB
CONFLICT OF INTEREST The authors declare no conflicts of interest.
Mathias Forkmann, MD e-mail: [email protected] Marian Christoph, MD Karim Ibrahim, MD Marko Swoboda, PhD Steffen Kolschmann, MD Ruth H. Strasser, PhD Carsten Wunderlich, MD Department of Cardiology Medical Clinic University of Technology Dresden, Germany
REFERENCES 1. Alexander JT, El-Ali AM, Newman JL, et al. Red blood cells stored for increasing periods produce progressive impairments in nitric oxide-mediated vasodilation. Transfusion 2013;53:2619-28. 2. Wang D, Sun J, Solomon SB, et al. Transfusion of older stored blood and risk of death: a meta-analysis. Transfusion 2012;52:1184-95. 3. Tinmouth A, Fergusson D, Yee IC, et al. Clinical consequences of red cell storage in the critically ill. Transfusion 2006;46:2014-27.
Anti-A and anti-B titers in group O platelet units are reduced in PAS C versus conventional plasma units Platelets (PLTs) stored in additive solution (PAS) remove a substantial fraction of plasma and replace it with an isotonic buffered solution. PAS C are apheresis PLTs stored in PAS 3 buffer (InterSol, Fenwal, Inc., a Fresenius-Kabi company, Lake Zurich, IL). PAS 3 is the first AS available in the United States and stores apheresis PLTs collected with the Amicus separator (Fenwal, Inc.) in a solution containing 65% PAS/35% plasma. Theoretically, this process should remove 65% of the plasma proteins, including isohemagglutinins. Transfusion of PLT units with high isohemagglutinin titers can pose a risk of hemolysis if the unit crosses ABO type. This risk is greater when group O PLTs are released to non-O patients. Many blood banks titer all O units and Volume 54, January 2014 TRANSFUSION
255
