Nitrite reductase activity of hemoglobin as a systemic nitric oxide generator mechanism to detoxify plasma hemoglobin produced during hemolysis

American Journal of Physiology - Heart and Circulatory Physiology - Tập 295 Số 2 - Trang H743-H754 - 2008
Peter C. Minneci1, Katherine J. Deans, Sruti Shiva, Zhi Huang, Steven M. Banks, Steven J. Kern, Charles Natanson, Steven B. Solomon, Mark T. Gladwin
1Department of Surgery, The Children's Institute for Surgical Science, The Children's Hospital of Philadelphia, PA, USA.

Tóm tắt

Hemoglobin (Hb) potently inactivates the nitric oxide (NO) radical via a dioxygenation reaction forming nitrate (NO3). This inactivation produces endothelial dysfunction during hemolytic conditions and may contribute to the vascular complications of Hb-based blood substitutes. Hb also functions as a nitrite (NO2) reductase, converting nitrite into NO as it deoxygenates. We hypothesized that during intravascular hemolysis, nitrite infusions would limit the vasoconstrictive properties of plasma Hb. In a canine model of low- and high-intensity hypotonic intravascular hemolysis, we characterized hemodynamic responses to nitrite infusions. Hemolysis increased systemic and pulmonary arterial pressures and systemic vascular resistance. Hemolysis also inhibited NO-dependent pulmonary and systemic vasodilation by the NO donor sodium nitroprusside. Compared with nitroprusside, nitrite demonstrated unique effects by not only inhibiting hemolysis-associated vasoconstriction but also by potentiating vasodilation at plasma Hb concentrations of <25 μM. We also observed an interaction between plasma Hb levels and nitrite to augment nitroprusside-induced vasodilation of the pulmonary and systemic circulation. This nitrite reductase activity of Hb in vivo was recapitulated in vitro using a mitochondrial NO sensor system. Nitrite infusions may promote NO generation from Hb while maintaining oxygen delivery; this effect could be harnessed to treat hemolytic conditions and to detoxify Hb-based blood substitutes.

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Tài liệu tham khảo

10.1378/chest.107.1.50

10.1074/jbc.M509045200

10.1038/nchembio.2007.46

10.1172/JCI19019

10.1098/rspb.1937.0057

10.1016/S0304-4165(98)00065-8

10.1085/jgp.42.1.83

Coin JT, Olson JS.The rate of oxygen uptake by human red blood cells.J Biol Chem254: 1178–1190, 1979.

10.1016/j.bpc.2007.03.004

10.1038/nm954

10.1182/blood-2005-07-2668

Davis CL, Kausz AT, Zager RA, Kharasch ED, Cochran RP.Acute renal failure after cardiopulmonary bypass in related to decreased serum ferritin levels.J Am Soc Nephrol10: 2396–2402, 1999.

10.1182/blood-2005-02-0567

10.1038/nbt0798-672

10.1016/S0301-4622(02)00090-X

10.1016/S0162-0134(00)80291-3

10.1016/S0002-8703(97)70091-7

10.1172/JCI22493

10.1002/ajh.10387

10.1038/288373a0

10.1152/ajpheart.00407.2006

10.1056/NEJMoa035477

10.1038/nchembio1105-308

10.1074/jbc.275.11.7757

10.1073/pnas.96.16.9027

10.1038/34402

10.1152/ajpheart.01172.2005

10.1152/jappl.1993.74.4.1769

10.3109/10731199409117867

10.1073/pnas.201276698

10.1074/jbc.M501496200

10.1016/S0304-4165(01)00227-6

10.1172/JCI24650

10.1038/nm1109

10.1073/pnas.84.24.9265

10.1161/01.RES.61.6.866

10.1016/0304-4165(80)90297-4

10.1152/ajpheart.00759.2007

10.1038/380221a0

10.1172/JCI9225

10.1172/JCI200421633

10.1161/01.ATV.0000204350.44226.9a

10.1016/S0014-5793(99)00788-7

10.1006/mvre.1996.0043

10.1074/jbc.M011648200

10.1073/pnas.96.15.8757

10.1074/jbc.273.30.18709

10.1074/jbc.M201939200

10.1136/gut.35.11.1543

10.1056/NEJM200307243490419

10.1016/S0014-5793(98)00430-X

10.1172/JCI25040

Mittal CK, Arnold WP, Murad F.Characterization of protein inhibitors of guanylate cyclase activation from rat heart and bovine lung.J Biol Chem253: 1266–1271, 1978.

Modin A, Bjorne H, Herulf M, Alving K, Weitzberg E, Lundberg JO.Nitrite-derived nitric oxide: a possible mediator of “acidic-metabolic” vasodilation.Acta Physiol Scand171: 9–16, 2001.

10.1111/j.1525-1594.1997.tb03747.x

10.1074/jbc.M307572200

10.1016/j.niox.2006.01.012

10.1093/ajcp/56.2.137

10.1182/blood-2005-04-1594

10.1152/ajpgi.00200.2004

10.1038/333664a0

10.1038/327524a0

10.3109/10715769409056556

10.1161/CIRCRESAHA.107.152488

10.1038/nm1202-799

10.1016/j.niox.2007.04.002

10.1001/jama.293.13.1653

10.1007/s002460010102

10.1097/00002480-199709000-00080

10.1161/01.RES.0000260171.52224.6b

10.1126/science.276.5321.2034

10.1006/niox.2000.0328

10.1074/jbc.275.4.2342

10.1152/ajpheart.1998.274.5.H1705

10.1182/blood-2006-12-061697

10.1073/pnas.0402927101

10.1159/000031200

10.1080/1071576021000033112

10.1161/CIRCULATIONAHA.107.729137

10.1038/nm0895-804