Endothelial NOS-derived nitric oxide prevents injury resulting from reoxygenation in the hypoxic lung

Abstract

To date, the role that NO derived from endothelial NO synthase (eNOS) plays in the development of the injuries occurring under hypoxia/reoxygenation (H/R) in the lung remains unknown and thus constitutes the subject of the present work. A follow-up study was conducted in Wistar rats submitted to H/R (hypoxia for 30 min; reoxygenation of 0 h, 48 h and 5 days), with or without prior treatment using the eNOS inhibitor L-NIO (20 mg/kg). Lipid peroxidation, apoptosis, protein nitration and NO production (NOx) were analysed. The results showed that L-NIO administration lowered NOx levels in all the experimental groups. Contrarily, the lipid peroxidation level and the percentage of apoptotic cells rose, implying that eNOS-derived NO may have a protective effect against the injuries occurring during H/R in the lung. These findings could open the possibility of future studies to design new therapies for this type of hypoxia based on NO-pharmacology.

Keywords::

• Hypoxia
• nitric oxide
• endothelial nitric oxide synthase
• L-NIO
• reoxygenation
• lipid peroxidation
• apoptosis

Acknowledgements

We wish to thank to Rafael Lomas for his statistic assistance and Mr David Nesbitt for his editorial help with the English version of the manuscript.

Declaration of interest: Supported by ‘MCyT’ (BIO 2000-0405-P4-05; SAF2003-04398-C02-02) and Junta de Andalucía (CVI-0184).