The Role of Nitric Oxide Synthase in Post-Operative Hyperglycaemia

• Main Author: Qader SS
• Format: Article
• Language: English
• Published: Taylor & Francis Group 2008-01-01
• Series: Libyan Journal of Medicine
• Subjects: NO; glucotoxicity; lipotoxicity; post-operative hyperglycaemia; pancreatic islets
• Online Access: http://www.ljm.org.ly/articles/AOP/AOP080416/AOP080416.pdf

Post-operative hyperglycaemia is important with regard to outcomes of surgical operations. It affects post-operative morbidity, length of hospital stay, and mortality. Poor peri-operative blood glucose control leads to a higher risk of post-operative complication. Insulin resistance as a cause of post-operative hyperglycaemia has been blamed for some time. Nitric Oxide (NO) is produced by nitric oxide synthase (NOS) isoenzymes. Inducible nitric oxide synthase (iNOS) is not a normal cellular constitute. It is expressed by cytokines and non-cytokines e.g. fasting, trauma, intravenous glucose, and lipid infusion, which are encountered in surgical operations. Review of current published data on postoperative hyperglycaemia was completed. Our studies and others were explored for the possible role of NO in this scenario. Induction and expression of iNOS enzyme in pancreatic islet cells is included in the chaotic postoperative blood glucose control. The high concentrations of iNOS derived NO are toxic to pancreatic β-cells and may inhibit insulin secretion postoperatively. Hence, current peri-operative management is questionable regarding post-operative hyperglycaemia and necessitates development of a new strategy.