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1 CNR Institute of Clinical Physiology, Faculty of Medicine, University of Pisa, Pisa, Italy
2 NicOx S.A., Sophia Antipolis, France
* To whom correspondence should be addressed. E-mail: sibert{at}ifc.cnr.it.
NCX 4016, aspirin which has been chemically combined with an NO donor, has been shown to inhibit cyclo-oxygenase and prostaglandin generation, while maintaining the inhibitory effects of aspirin. The possible role of reactive oxygen species (ROS) in the action of NCX 4016 in ischemia-reperfusion (I/R) has not been studied. Furthermore, we were interested in comparing the effects of a conventional NO donor (2,2'-hydroxynitrosohydrazino- bis-etanamine, DETA/NO) and NCX 4016 at the microvascular level in the hamster cheek pouch visualized by using an intravital fluorescent microscopy technique. Microvascular injury was assessed by measuring diameter change, the perfused capillary length (PCL) and leukocyte adhesion. Animals were treated with NCX 4016 (10 mg/100 g or 3 mg/100 g/day for five days, orally administered) or (DETA-NO) (0.05 mg/100 g, intravenously injected). Mean arterial blood pressure increased slightly but significantly after NCX 4016 treatment. During 5- and 15-min reperfusion, lipid peroxides in the systemic blood increased by 72 and 89% vs. baseline respectively, and were still higher than in basal conditions after 30-min reperfusion in the I/R group. Pretreatment with NCX 4016 maintained ROS at normal levels, increased arteriolar diameter, blood flow and PCL, and decreased leukocyte adhesion (p < 0.05). DETA-NO decreased ROS during 30-min reperfusion, later however, there was a significant increase during reperfusion. DETA-NO decreased leukocyte adhesion (p < 0.05) but microvascular permeability increased after 30 min of reperfusion. In conclusion, NCX 4016 attenuates oxidative stress and prevents arteriolar constriction during I/R while DETA-NO increases lipid peroxides in the systemic blood and permeability after reperfusion.
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