Related Experiment Videos
Differential nitric oxide synthase expression during hepatic ischemia-reperfusion
Ferdinand Serracino-Inglott1, Ioannis T Virlos, Nagy A Habib
1Division of Surgery, Anesthetics and Intensive Care, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom. fsinglott@hotmail.com
American Journal of Surgery
|June 5, 2003
Summary
Hepatic ischemia-reperfusion injury involves decreased endothelial nitric oxide synthase and increased inducible nitric oxide synthase. This study shows inducible nitric oxide synthase expression contributes to liver injury during reperfusion.
Area of Science:
- Hepatology
- Biochemistry
- Immunology
Background:
- Nitric oxide plays a critical role in hepatic ischemia-reperfusion injury.
- Reperfusion injury is linked to reduced nitric oxide from endothelial nitric oxide synthase and increased nitric oxide from inducible nitric oxide synthase.
Purpose of the Study:
- To characterize the expression of endothelial and inducible nitric oxide synthase isoforms during hepatic reperfusion.
- To investigate the role of nitric oxide synthase isoforms in mediating liver injury after ischemia-reperfusion.
Main Methods:
- Male Wistar rats underwent partial hepatic ischemia followed by reperfusion.
- Immunohistochemistry and Western blotting assessed nitric oxide synthase isoform expression.
- Nitrotyrosine staining identified protein damage from peroxynitrite.
Main Results:
- Control livers showed normal endothelial nitric oxide synthase and no inducible nitric oxide synthase expression.
- Ischemic livers exhibited decreased endothelial nitric oxide synthase and inducible nitric oxide synthase expression in hepatocytes and inflammatory cells.
- Nitrotyrosine staining was observed in ischemic livers, indicating peroxynitrite formation.
Conclusions:
- Endothelial nitric oxide synthase is downregulated, while inducible nitric oxide synthase is upregulated during hepatic reperfusion.
- Inducible nitric oxide synthase expression in hepatocytes and inflammatory cells contributes to hepatic ischemia-reperfusion injury.
- Nitric oxide synthase isoform modulation is a key factor in liver reperfusion injury pathogenesis.