Nitric Oxide Metabolite Levels in Acute Vaso‐occlusive Sickle‐cell Crisis
Open Access
- 1 December 1996
- journal article
- Published by Wiley in Academic Emergency Medicine
- Vol. 3 (12) , 1098-1102
- https://doi.org/10.1111/j.1553-2712.1996.tb03367.x
Abstract
Objectives: 1) To measure nitric oxide (NO) metabolite levels in patients presenting to the ED in acute vasoocclusive sickle-cell crisis (SCC), and 2) to determine whether a relationship exists between NO metabolite levels and pain. Methods: A prospective, observational study of patients with documented sickle-cell anemia (SCA), aged ±18 years, presenting in typical, acute SCC was conducted in an urban, university teaching hospital. Excluded were those with atypical pain or acute, coexistent disease (as evidenced by fever, tachycardia, tachyon, or hypotension). Pain scores were measured by a 10-cm visual analog scale (VAS). Blood NO metabolite levels for SCC patients and control subjects (healthy volunteers, n = 9; SCA control subjects not in SCC, n = 10) were determined using an NO-specific chemiluminescence technique that measured plasma nitrite and nitrate, the stable end-products of NO. The acute SCC patients were divided into 3 groups, with the range for the SCC-normal (n = 5) group defined as within 2 SD of the healthy volunteer control patients. The SCC-low patients (n = 21) had NO metabolite levels below this range and the SCC-high (n = 21) patients had levels above this range. Results: The SCA and healthy volunteer control groups had similar NO metabolite levels (25.3 vs 22.6 μmol; p = 0.10). The 3 acute SCC groups had the following mean NO levels: 1) SCC-normal = 21.3 ± 1.6 μmol; 2) SCC-low = 7.2 ± 1.1 μmol; and 3) SCC-high = 43.7 ± 3.5 μmol. The SCC-high NO-level group had significantly lower VAS pain scores when compared with the SCC-low and SCC-normal NO-level groups (6.52 ± 1.85 cm vs 8.76 ± 0.83 cm, and 8.62 ± 1.29 cm, p = 0.02). Conclusion: NO metabolite levels vary in SCC patients. Elevated levels are associated with lower pain scores, while lower levels are associated with higher pain scores, indicating that NO metabolites may potentially represent a marker for compensatory mechanisms in SCC tissue ischemia. Further work is needed to delineate the usefulness of NO metabolites in assessing the seventy of SCC.Keywords
This publication has 29 references indexed in Scilit:
- Pharmacodynamics of Plasma Nitrate/Nitrite as an Indication of Nitric Oxide Formation in Conscious DogsCirculation, 1995
- Plasma nitrate concentrations in neutropenic and non‐neutropenic patients with suspected septicaemiaBritish Journal of Haematology, 1995
- Effect of topical administration of l‐arginine on formalin‐induced nociception in the mouse: a dual role of peripherally formed NO in pain modulationBritish Journal of Pharmacology, 1994
- Carvedilol, a new antihypertensive agent, prevents lipid peroxidation and oxidative injury to endothelial cells.Hypertension, 1993
- Role of nitric oxide in maintaining vascular integrity in endotoxin‐induced acute intestinal damage in the ratBritish Journal of Pharmacology, 1990
- The crucial role of physiological Ca2+ concentrations in the production of endothelial nitric oxide and the control of vascular toneBritish Journal of Pharmacology, 1990
- Endothelium-derived relaxing factor produced and released from artery and vein is nitric oxide.Proceedings of the National Academy of Sciences, 1987
- ENDOGENOUS NITRIC OXIDE INHIBITS HUMAN PLATELET ADHESION TO VASCULAR ENDOTHELIUMPublished by Elsevier ,1987
- Advances continue in sickle cell diseasePublished by American Medical Association (AMA) ,1982
- The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholineNature, 1980