Sodium nitroprusside as a nitric oxide donor in a rat intestinal ischemia reperfusion model: a novel molecular mechanism

LETTER TO THE EDITOR

Sodium nitroprusside as a nitric oxide donor in a rat intestinal ischemia reperfusion model: a novel molecular mechanism

Hamid Namazi

Chamran Hospital, Shiraz University of Medical Sciences – Shiraz, Islamic Republic of Iran. [e-mail]

I have read with great interest the article by Emre et al.¹ Their work showed that sodium nitroprusside could be elegantly used to reduce intestinal ischemia reperfusion. This is underscored by a decrease in inflammation as compared to using a placebo. I would like to further discuss this article by introducing a major route through which sodium nitroprusside could suppress inflammation.

The recent focus on ischemia-reperfusion injury has been on the interaction between neutrophils and endothelial cells. Transendothelial migration of neutrophils, with release of reactive oxygen species and cytokines, causes further damage to the injured tissue.^2,3 However, key components in the pathogenesis of reperfusion syndrome include the up-regulation of surface adhesion molecules on the vascular endothelium and their subsequent interaction with activated neutrophils.⁴ The most important adhesion protein identified on neutrophils is the integrin lymphocyte function-associated antigen-1 (LFA-1; CD11a/CD18). This is the ligand for intercellular adhesion molecule-1 (ICAM-1), which is expressed on the endothelium. The LFA-1/ICAM-1 interaction is crucial for neutrofils to ingress into inflammatory sites.^5,6 Sodium nitroprusside down-regulates ICAM-1 and LFA-1 expression, and interferes with the ICAM-1–LFA-1 interaction by binding to LFA-1.^7,8 This important mechanism should be borne in mind as the major mechanism for sodium nitroprusside-induced inhibition of neutrophil activity.

• 1. Emre A, Bayram O, Salman B, Ercan S, Anadol Z, Akin O. Sodium nitroprusside as a nitric oxide donor in a rat intestinal ischemiareperfusion model. Clinics. 2008;63:91-6.
• 2. Ozacmak VH, Sayan H. Pretreatment with adenosine and adenosine A1 receptor agonist protects against intestinal ischemia-reperfusion injury in rat. World J Gastroenterol. 2007;13:538-47.
• 3. Barut I, Tarhan OR, Kapucuoglu N, Sutcu R, Akdeniz Y. Lamotrigine reduces intestinal I/R injury in the rat. Shock. 2007;28:202-6.
• 4. Tosa Y, Lee WP, Kollias N, Randolph MA, May JW Jr.. Monoclonal antibody to intercellular adhesion molecule 1 protects skin flaps against ischemia-reperfusion injury: an experimental study in rats. Plast Reconstr Surg. 1998;101:1586-94.
• 5. Haskard DO and Lee TH. The role of leukocyte-endotheial interactions in the accumulation of leukocytes in allergic inflammation. Am Rev Respir Dis. 1992;145:10-13.
• 6. Chen PL, Easton A. Apoptotic Phenotype Alters the Capacity of Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand to Induce Human Vascular Endothelial Activation. J Vasc Res. 2007;45:111-22.
• Exp Cell Res. 1997;235:431-4.
• 8. Ikeda M, Ikeda U, Takahashi M, Shimada K, Minota S, Kano S. Nitric oxide inhibits intracellular adhesion molecule-1 expression in rat mesangial cells. J Am Soc Nephrol. 1996;7:2213-8.

Publication Dates

• Publication in this collection
  17 June 2008
• Date of issue
  2008