| Artery-to-vein differences in nitric oxide metabolites are diminished in sepsis. | |
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MedLine Citation:
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PMID: 20081526 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: Nitric oxide deficiency may contribute to microvascular dysfunction in sepsis. Current physiologic paradigms contend that nitrite and/or S-nitrosohemoglobin mediate intravascular delivery of nitric oxide. These nitric oxide metabolites are purportedly consumed during hemoglobin deoxygenation, producing nitric oxide and coupling intravascular nitric oxide delivery with metabolic demand. Systemic nitrite and S-nitrosohemoglobin consumption can be assessed by comparing their concentrations in arterial vs. venous blood. We hypothesized that arterial vs. venous differences in nitrite and S-nitrosohemoglobin are diminished in sepsis and associated with mortality. DESIGN: Case-control and prospective cohort study. SETTING: Adult intensive care units of an academic medical center. PATIENTS AND SUBJECTS: Eighty-seven critically ill septic patients and 52 control subjects. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Nitrite and S-nitrosohemoglobin were measured using tri-iodide-based reductive chemiluminescence. In control subjects, arterial plasma, whole blood, and red blood cell nitrite levels were higher than the corresponding venous levels. In contrast, S-nitrosohemoglobin was higher in venous compared to arterial blood. In septic patients, arterial vs. venous red blood cell nitrite and S-nitrosohemoglobin differences were absent. Furthermore, the plasma nitrite arterial vs. venous difference was absent in nonsurvivors. CONCLUSIONS: In health, nitrite levels are higher in arterial vs. venous blood (suggesting systemic nitrite consumption), whereas S-nitrosohemoglobin levels are higher in venous vs. arterial blood (suggesting systemic S-nitrosohemoglobin production). These arterial vs. venous differences are diminished in sepsis, and diminished arterial vs. venous plasma nitrite differences are associated with mortality. These data suggest pathologic disruption of systemic nitrite utilization in sepsis. |
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Authors:
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Mary Anne M Morgan; Lauren M Frasier; Judith C Stewart; Cynthia M Mack; Michael S Gough; Brian T Graves; Michael J Apostolakos; Kathleen P Doolin; Denise C Darling; Mark W Frampton; Anthony P Pietropaoli |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: Critical care medicine Volume: 38 ISSN: 1530-0293 ISO Abbreviation: Crit. Care Med. Publication Date: 2010 Apr |
Date Detail:
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Created Date: 2010-03-25 Completed Date: 2010-04-09 Revised Date: 2012-10-09 |
Medline Journal Info:
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Nlm Unique ID: 0355501 Medline TA: Crit Care Med Country: United States |
Other Details:
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Languages: eng Pagination: 1069-77 Citation Subset: AIM; IM |
Affiliation:
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Departments of Medicine, University of Rochester Medical Center, Rochester, NY, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Age Factors Aged Arteries / metabolism*, physiopathology Case-Control Studies Cohort Studies Female Hemoglobins / analysis Hospital Mortality Humans Luminescent Measurements Male Middle Aged Nitric Oxide / blood, metabolism* Nitrites / blood Prospective Studies Sepsis / blood*, mortality, physiopathology Veins / metabolism*, physiopathology |
| Grant Support | |
ID/Acronym/Agency:
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K23 HL080077-05/HL/NHLBI NIH HHS; K23 HL80077/HL/NHLBI NIH HHS; UL1 RR 024160/RR/NCRR NIH HHS; UL1 RR024160/RR/NCRR NIH HHS; UL1 RR024160-05/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Hemoglobins; 0/Nitrites; 0/S-nitrosohemoglobin; 10102-43-9/Nitric Oxide |
| Comments/Corrections | |
Comment In:
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Crit Care Med. 2010 Apr;38(4):1214-5
[PMID:
20335702
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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