Storage lesion: role of red blood cell breakdown

Transfusion - Tập 51 Số 4 - Trang 844-851 - 2011
Daniel B. Kim‐Shapiro1,2, Janet Lee1,2, Mark T. Gladwin1,2
1From the Department of Physics and the Translational Science Center, Wake Forest University, Winston-Salem, North Carolina
2the Vascular Medicine Institute and the Department of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania.

Tóm tắt

As stored blood ages intraerythrocytic energy sources are depleted resulting in reduced structural integrity of the membrane. Thus, stored red blood cells (RBCs) become less deformable and more fragile as they age. This fragility leads to release of cell‐free hemoglobin (Hb) and formation of microparticles, submicron Hb‐containing vesicles. Upon transfusion, it is likely that additional hemolysis and microparticle formation occurs due to breakdown of fragile RBCs. Release of cell‐free Hb and microparticles leads to increased consumption of nitric oxide (NO), an important signaling molecule that modulates blood flow, and may promote inflammation. Stored blood may also be deficient in recently discovered blood NO synthase activity. We hypothesize that these factors play a potential role in the blood storage lesion.

Từ khóa


Tài liệu tham khảo

Dern RJ, 1967, Studies on the preservation of human blood. II. The relationship of erythrocyte adenosine triphosphate levels and other in vitro measures to red cell storageability, J Lab Clin Med, 69, 968

Silliman CC, 1994, Partial characterization of lipids that develop during the routine storage of blood and prime the neutrophil NADPH oxidase, J Lab Clin Med, 124, 684

10.1046/j.1537-2995.1988.28488265266.x

10.1046/j.1537-2995.1982.22282177126.x

10.1111/j.1423-0410.1990.tb02068.x

10.1016/0003-9861(68)90114-8

10.1111/j.1537-2995.1969.tb05527.x

10.1172/JCI105987

10.1016/S0140-6736(07)61197-0

10.1006/jsre.2001.6306

10.1111/j.1537-2995.1969.tb04929.x

10.1046/j.1365-3148.2000.00267.x

Izzo P, 1999, Erythrocytes stored in CPD SAG‐mannitol: evaluation of their deformability, Clin Hemorheol Microcirc, 21, 335

10.1046/j.1537-2995.1982.22282177134.x

10.1111/j.1365-2141.1983.tb02016.x

10.1182/blood.V71.2.448.448

10.1111/j.1537-2995.2007.01549.x

10.1111/j.1423-0410.1991.tb00920.x

10.1083/jcb.73.3.548

10.1111/j.1537-2995.2006.01026.x

10.1016/S0002-9610(99)00239-1

10.1001/archsurg.1997.01430300062013

10.1001/jama.1993.03500230106037

10.1001/archsurg.137.6.711

10.1007/BF03012772

10.1097/00000542-200304000-00005

10.1056/NEJMoa070403

10.1097/01.CCM.0000108878.23703.E0

10.1097/00000542-200304000-00003

10.1056/NEJMe0800520

10.1046/j.1537-2995.2000.40010101.x

10.1111/j.1537-2995.2006.00958.x

10.1111/j.1537-2995.2010.02583.x

10.1016/j.transci.2010.05.013

10.1038/nm0410-381

10.1038/288373a0

10.1161/01.RES.61.6.866

Katsuki S, 1977, Stimulation of guanylate cyclase by sodium nitroprusside, nitroglycerin and nitric‐oxide in various tissue preparations and comparison to effects of sodium azide and hydroxylamine, J Cyclic Nucleotide Res, 3, 23

10.1038/327524a0

10.1074/jbc.M310141200

10.1016/S0005-2728(99)00028-6

Ignarro LJ, 2000, Nitric oxide biology and pathobiology

10.1182/blood-2005-10-3992

10.1016/S0162-0134(00)80291-3

10.1021/bi960442g

10.1021/bi002407m

10.1073/pnas.91.17.8137

10.1085/jgp.42.1.83

Coin JT, 1979, Rate of oxygen‐uptake by human red blood‐cells, J Biol Chem, 254, 1178, 10.1016/S0021-9258(17)34185-6

10.1016/S0304-4165(98)00065-8

Vaughn MW, 1998, Estimation of nitric oxide production and reaction rates in tissue by use of a mathematical model, Am J Physiol Heart Circ Physiol, 43, H2163, 10.1152/ajpheart.1998.274.6.H2163

10.1073/pnas.96.15.8757

10.1074/jbc.275.4.2342

10.1006/niox.2000.0328

10.1074/jbc.M201939200

10.1073/pnas.201276698

10.1074/jbc.273.30.18709

10.1074/jbc.M509045200

Vaughn MW, 1998, Effective diffusion distance of nitric oxide in the microcirculation, Am J Physiol Heart Circ Physiol, 43, H1705, 10.1152/ajpheart.1998.274.5.H1705

10.1161/01.ATV.0000204350.44226.9a

Kevil CG, 2010, S‐Nitrosothiol biology and therapeutic potential in metabolic disease, Curr Opin Investig Drugs, 11, 1127

10.1111/j.1463-1326.2010.01267.x

10.1007/s00424-010-0796-2

10.1016/j.maturitas.2010.04.006

10.32725/jab.2009.019

10.1001/jama.293.13.1653

10.1152/jappl.1993.74.4.1769

10.1152/jappl.1995.79.1.236

Vogel WM, 1986, Coronary constrictor effect of stroma‐free hemoglobin‐solutions, Am J Physiol, 251, H413

10.1016/0016-5085(95)90584-7

10.1038/nm1202-799

10.1172/JCI25040

10.1016/j.freeradbiomed.2006.08.017

10.1182/blood-2005-08-3285

10.1182/blood-2005-06-2373

10.1182/blood-2005-04-1594

10.1056/NEJMoa035477

10.1001/jama.294.1.81

10.1182/blood-2010-04-282095

10.1182/blood-2010-02-268193

10.1097/MOH.0b013e32833157f4

10.1016/j.bbagen.2005.01.013

10.1182/blood-2009-10-245001

10.1182/blood-2008-07-166264

10.1182/blood.V100.3.879

10.1111/j.1537-2995.2010.02861.x

10.1111/j.1365-2141.2008.07155.x

10.1172/JCI116706

10.1126/science.1181928

10.1172/JCI112582

10.1182/blood-2006-12-061697

10.1084/jem.20041497

10.1182/blood.V98.6.1802

10.1056/NEJM199902113400601

10.1126/scitranslmed.3001118

10.1016/j.niox.2008.02.006

10.1038/nm954