Effects of S-nitrosation on hemoglobin-induced microvascular damage.
Antioxid Redox Signal
; 8(7-8): 1093-101, 2006.
Article
em En
| MEDLINE
| ID: mdl-16910757
ABSTRACT
Blood substitutes, such as diaspirin cross-linked hemoglobin (Hb), cause microvascular leakiness to macromolecules. Because of the potentially stabilizing effects of nitric acid (NO) on endothelium, experiments were performed to determine whether S-nitrosohemoglobin (SNO-Hb), a potential NO-donor Hb-based blood substitute, would not cause microvascular damage. Release of NO, or its metabolites, from the SNO-Hb was facilitated by addition of glutathione, which aids in the decomposition of S-nitrosothiols. In anesthetized rats, the mesenteric microvasculature was perfused with SNO-Hb with glutathione (six rats), SNO-Hb alone (six rats), or saline (eight rats) for 10 min, followed by fluorescein isothiocyanate (FITC)-albumin for 1 min, and finally fixed for epifluorescence microscopic examination. When comparing the SNO-Hb group with saline, both the numbers and areas of leaks were significantly increased [0.019 +/- 0.003 (SEM) microm vs. 0.0030 +/- 0.0004 and 7.36 +/- 1.50 vs. 0.156 +/- 0.035 (p < 0.005)]. With the addition of glutathione, leakage was still high (0.005 +/- 0.00005 microm and 5.086 +/- 0.064 microm) but decreased compared with SNO-Hb alone (p < 0.005). In conclusion, NO, or a related vasodilator, when released from SNO-Hb, significantly reduces but does not eliminate microvascular damage. Further improvements may result by S-nitrosating a more stable form of modified hemoglobin.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Substitutos Sanguíneos
/
Hemoglobinas
/
Aspirina
/
Mucosa Intestinal
/
Nitratos
Limite:
Animals
Idioma:
En
Revista:
Antioxid Redox Signal
Assunto da revista:
METABOLISMO
Ano de publicação:
2006
Tipo de documento:
Article
País de afiliação:
Estados Unidos