抄録
We determined the changes in hepatic sinusoidal pressure and liver weight, and the effects of a NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) in ischemia-reperfusion (I/R) injury of isolated mouse livers perfused portally with diluted blood (Hct 3%). Following pretreatment with L-NAME (100 μM) or D-NAME (100 μM), Ischemia was induced at room temperature by occlusion of the inflow line of the portal vein for 1 hour, followed by 1-hour reperfusion in a recirculating manner. The sinusoidal pressure was assessed by the double vascular occlusion pressure (Pdo). In the D-NAME group, immediately after reperfusion, the portal pressure increased by 2.8±0.1(SE) mmHg, which was accompanied by an increase in Pdo by 1.5±0.1 mmHg, suggesting increases in pre- and post-sinusoidal resistances in a similar degree. Liver weight increased 0.14±0.04 g after reperfusion followed by a gradual return towards baseline. Liver injury, assessed by perfusate levels of hepatic enzymes was observed at 60 min after reperfusion. There were no significant differences in changes in any variables between the D- and L-NAME groups. In conclusion, the increases in both the hepatic vascular resistances and the sinusoidal pressure were small in magnitude, resulting in absence of edematous changes in mouse hepatic I/R, and nitric oxide does not play any significant roles in this injury. [J Physiol Sci. 2006;56 Suppl:S134]
