Sickle Cell Anemia Research Today is a free monthly online journal that collates and summarizes the latest research about Sickle Cell Anemia, including details on genetics, causes, symptoms.

Protective effects of S-nitrosoalbumin on lung injury induced by hypoxia-reoxygenation in mouse model of sickle cell disease.

de Franceschi L, Malpeli G, Scarpa A, Janin A, Muchitsch EM, Roncada P, Leboeuf C, Corrocher R, Beuzard Y, Brugnara C

Section of Internal Medicine, Department of Clinical and Experimental Medicine, University of Verona, Italy. lucia.defranceschi@univr.it

Nitric oxide (NO) is a potential new therapeutic agent for sickle cell disease (SCD). We investigated the effects of NO donor on hypoxia-induced acute lung injury that occurs when transgenic sickle cell SAD mice are exposed to chronic hypoxia, a model for lung vasoocclusive sickle cell events. In wild-type and SAD mice, intraperitoneal injection of S-nitrosoalbumin (NO-Alb) produced no significant hematologic changes under room air conditions, whereas it induced mild temporary hypotension and inhibition of platelet aggregation. NO-Alb administration (300 mg/kg ip twice a day, equivalent to 7.5 microM NO) in wild-type and SAD mice exposed to 46 h of hypoxia (8% oxygen) followed by 2 h of normoxia resulted in 1) reduction of the hypoxia-induced increase in blood neutrophil count, 2) prevention of hypoxia-induced increased IL-6 and IL-1beta levels in bronchoalveolar lavage, 3) reduction of the lung injury induced by hypoxia-reoxygenation, 4) prevention of thrombus formation, and 5) prevention of hypoxia-induced increase of lung matrix metalloproteinase-9 gene expression. These effects provide new insights into the possible use of NO-Alb in the treatment of acute lung injury in SCD.

Published 10 August 2006 in Am J Physiol Lung Cell Mol Physiol, 291(3): L457-65.
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