AI Article Synopsis
- - Preconditioning with brief ischemia-reperfusion (I/R) enhances the protection of coronary endothelial cells from injury caused by later reperfusion, indicating a potential protective mechanism.
- - In a study with anesthetized rats, different NO synthase inhibitors were used to analyze their effects on the protection seen during prolonged I/R, specifically targeting the role of nitric oxide.
- - Results showed that the general NOS inhibitor l-NAME blocked the protective effects of preconditioning, suggesting that nitric oxide produced by endothelial NOS (eNOS) is crucial for delayed endothelial protection during I/R events.
Article Abstract
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 x 2-min ischemia/5-min reperfusion and 2 x 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.
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| http://dx.doi.org/10.1152/ajpheart.00627.2002 | DOI Listing |
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