| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
INFLAMMATION/IMMUNITY/MEDIATORS
1Consiglio Nazionale della Ricerca Institute of Clinical Physiology, Faculty of Medicine, University of Pisa, 56100 Pisa, Italy; and 2NicOx S.A., Sophia Antipolis 06906, France
Submitted 7 August 2003 ; accepted in final form 8 October 2003
Aspirin that has been chemically combined with a nitric oxide (NO) donor (NCX-4016) has been shown to inhibit cyclooxygenase 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 (100 mg/kg or 30 mg·kg-1·day-1 for 5 days po) or DETA-NO (0.5 mg/kg). 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; however, later 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, whereas DETA-NO increases lipid peroxides in the systemic blood and permeability after reperfusion.
oxidative stress; nitric oxide-aspirin; microcirculation; lipid peroxides
This article has been cited by other articles:
|
|
 |
|
  S. Bertuglia Intermittent hypoxia modulates nitric oxide-dependent vasodilation and capillary perfusion during ischemia-reperfusion-induced damage Am J Physiol Heart Circ Physiol, April 1, 2008; 294(4): H1914 - H1922. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Bertuglia, F. M. Veronese, and G. Pasut Polyethylene glycol and a novel developed polyethylene glycol-nitric oxide normalize arteriolar response and oxidative stress in ischemia-reperfusion Am J Physiol Heart Circ Physiol, October 1, 2006; 291(4): H1536 - H1544. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. W. Park, W.-N. Qi, Y. Cai, I. Zelko, J. Q. Liu, L.-E. Chen, J. R. Urbaniak, and R. J. Folz Skeletal muscle reperfusion injury is enhanced in extracellular superoxide dismutase knockout mouse Am J Physiol Heart Circ Physiol, July 1, 2005; 289(1): H181 - H187. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Bertuglia and A. Giusti Role of nitric oxide in capillary perfusion and oxygen delivery regulation during systemic hypoxia Am J Physiol Heart Circ Physiol, February 1, 2005; 288(2): H525 - H531. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Bertuglia and A. Giusti Role of nitric oxide in capillary perfusion and oxygen delivery regulation during systemic hypoxia Am J Physiol Heart Circ Physiol, February 1, 2005; 288(2): H525 - H531. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
