Nitric oxide synthase distribution and expression with ischemic preconditioning of the rat liver Rahul S. Koti * ,† , Janice Tsui * , Edgar Lobos ‡ , Wenxuan Yang * , Alexander M. Seifalian * ,† ,1 and Brian R. Davidson * ,† * Academic Division of Surgical and Interventional Sciences, University College London, London, UK; † Department of Surgery and Liver Transplantation Unit, Royal Free Hampstead NHS Trust Hospital, London, UK; and ‡ Institute of Anatomy, University of Leipzig, Leipzig, Germany 1 Correspondence: Academic Division of Surgical and Interventional Sciences, University College London, Rowland Hill St., London NW3 2PF, UK. E-mail: a.seifalian@medsch.ucl.ac.uk <h3>SPECIFIC AIM</h3> The aim of this study was to identify nitric oxide synthase isoforms responsible for generation of the cytoprotective effect of nitric oxide during liver ischemic preconditioning in a rat model of lobar ischemia reperfusion injury. <h3>PRINCIPAL FINDINGS</h3> <h3>1) Ischemia reperfusion (IR) results in decreased eNOS expression and increased hepatocellular injury</h3> To determine extent of liver injury with ischemia and reperfusion, rats were subjected to 45 min of lobar ischemia followed by 2 h of reperfusion (IR). This resulted in decreased NO production [3.4±0.4 µM (IR) vs. 15.5±1.7 µM (sham) P <0.05]. IR was
/lp/fed-of-american-socs-for-experimental-biology/nitric-oxide-synthase-distribution-and-expression-with-ischemic-2cUmCCqfzT