作者: Rahul S Koti , Wenxuan Yang , Michael R Dashwood , Brian R Davidson , Alexander M Seifalian
关键词: Pharmacology 、 Ischemic preconditioning 、 Nitric oxide 、 Ischemia 、 Anesthesia 、 Transplantation 、 Reperfusion injury 、 Nitric oxide synthase 、 Medicine 、 Endothelium 、 Liver injury
摘要: Ischemic preconditioning (IPC) may protect the liver from ischemia reperfusion injury by nitric oxide formation. This study has investigated effect of ischemic on hepatic microcirculation (HM), and relationship between metabolism HM in preconditioning. Rats were allocated to 5 groups: 1. sham laparotomy; 2. 45 minutes lobar followed 2-hour (IR); 3. IPC with 10 before IR; 4. L-arginine 5. L-NAME + IR. was monitored laser Doppler flowmeter. Liver transaminases, adenosine triphosphate, nitrites nitrates, guanosine 3'5'-cyclic monophosphate (cGMP) measured. Nitric synthase (NOS) distribution studied using nicotinamide adeninine dinucleotide phosphate (NADPH) diaphorase histochemistry. At end phase, IR group, flow recovered partially 25.8% baseline (P < .05 versus sham), whereas improved 49.5% .01 IR). With treatment, 31.6% (NS IR), showing no attenuation injury. In preconditioned group treated L-NAME, declined 10.2% baseline, suggesting not only a blockade effect, but also an exacerbated Hepatocellular reduced IPC, increased NO inhibition L-NAME. nitrate (NOx) cGMP concentrations. NOS detected NADPH staining associated hepatocytes vascular endothelium, induced IPC. attenuated impairment hepatocellular These data strongly suggest role for