| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Institut National de la Santé et de la Recherche Médicale E9920, Institut Fédératif de Recherches Multidisciplinaires sur les peptides 23, Department of Pharmacology, Rouen University Medical School, Rouen 76183, France
Preconditioning with brief periods of ischemia-reperfusion (I/R) induces a delayed protection of coronary endothelial cells against reperfusion injury. We assessed the possible role of nitric oxide (NO) produced during prolonged I/R as a mediator of this endothelial protection. Anesthetized rats were subjected to 20-min cardiac ischemia/60-min reperfusion, 24 h after sham surgery or cardiac preconditioning (1 × 2-min ischemia/5-min reperfusion and 2 × 5-min ischemia/5-min reperfusion). The nonselective NO synthase (NOS) inhibitor L-NAME, the selective inhibitors of neuronal (7-nitroindazole) or inducible (1400W) NOS, or the peroxynitrite scavenger seleno-L-methionine were administered 10 min before prolonged ischemia. Preconditioning prevented the reperfusion-induced impairment of coronary endothelium-dependent relaxations to acetylcholine (maximal relaxation: sham 77 ± 3; I/R 44 ± 6; PC 74 ± 5%). This protective effect was abolished by L-NAME (41 ± 7%), whereas 7-NI, 1400W or seleno-L-methionine had no effect. The abolition of preconditioning by L-NAME, but not by selective nNOS or iNOS inhibition, suggests that NO produced by eNOS is a mediator of delayed endothelial preconditioning.
coronary circulation; endothelial function; nitric oxide; peroxynitrite
This article has been cited by other articles:
|
|
 |
|
  A. Bellis, D. Castaldo, V. Trimarco, M. G. Monti, P. Chivasso, J. Sadoshima, B. Trimarco, and C. Morisco Cross-Talk Between PKA and Akt Protects Endothelial Cells From Apoptosis in the Late Ischemic Preconditioning Arterioscler Thromb Vasc Biol, August 1, 2009; 29(8): 1207 - 1212. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Mulder, V. Mellin, J. Favre, M. Vercauteren, I. Remy-Jouet, C. Monteil, V. Richard, S. Renet, J. P. Henry, A. Y. Jeng, et al. Aldosterone synthase inhibition improves cardiovascular function and structure in rats with heart failure: a comparison with spironolactone Eur. Heart J., September 1, 2008; 29(17): 2171 - 2179. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S.-J. Kim, X. Zhang, X. Xu, A. Chen, J. B. Gonzalez, S. Koul, K. Vijayan, G. J. Crystal, S. F. Vatner, and T. H. Hintze Evidence for enhanced eNOS function in coronary microvessels during the second window of protection Am J Physiol Heart Circ Physiol, May 1, 2007; 292(5): H2152 - H2158. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Yamaguchi, K. Kamada, C. Dayton, F. S. Gaskin, M. Yusof, T. Yoshikawa, P. Carter, and R. J. Korthuis Role of eNOS-derived NO in the postischemic anti-inflammatory effects of antecedent ethanol ingestion in murine small intestine Am J Physiol Heart Circ Physiol, March 1, 2007; 292(3): H1435 - H1442. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Ii, H. Nishimura, A. Iwakura, A. Wecker, E. Eaton, T. Asahara, and D. W. Losordo Endothelial Progenitor Cells Are Rapidly Recruited to Myocardium and Mediate Protective Effect of Ischemic Preconditioning via "Imported" Nitric Oxide Synthase Activity Circulation, March 8, 2005; 111(9): 1114 - 1120. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
