The aim of this study was to characterize the relationship between ischemia/reperfusion-induced liver injury and blood oxygen radical, nitric oxide (NO) and adenosine triphosphate (ATP). Ischemia was induced by clamping off the common hepatic artery and portal vein for 40 min, after which flow was restores, and the liver was reperfused for 90 min. Blood samples collected prior to ischemia and after reperfusion showed that this protocol resulted in elevated of blood NO levels (p<0.01), which were associated with diminished blood pressure (p<0.01). Inflammation was apparent, as white cell counts and levels of methyl guanidine, an oxygen radical reaction product, were both significantly increased (p<0.05 & p<0.001). Blood levels of SGOT, SGPT and LDH, which served as indexes of liver injury, were elevated 4 to 5 fold (p<0.001), while levels of ATP were significantly diminished (p<0.01). These findings make it likely that peroxynitric acid, the reaction product of NO and superoxide, as well as other reactive species are major factors involved in ischemia/reperfusion-induced liver injury.
The aim of this study was to characterize the relationship between ischemia/reperfusion-induced liver injury and blood oxygen radical, nitric oxide (NO) and adenosine triphosphate (ATP). Ischemia was induced by clamping off the common hepatic artery and portal vein for 40 min, after which flow was restores, and the liver was reperfused for 90 min. Blood samples collected prior to ischemia and after reperfusion showed that this protocol resulted in elevated of blood NO levels (p<0.01), which were associated with diminished blood pressure (p<0.01). Inflammation was apparent, as white cell counts and levels of methyl guanidine, an oxygen radical reaction product, were both significantly increased (p<0.05 & p<0.001). Blood levels of SGOT, SGPT and LDH, which served as indexes of liver injury, were elevated 4 to 5 fold (p<0.001), while levels of ATP were significantly diminished (p<0.01). These findings make it likely that peroxynitric acid, the reaction product of NO and superoxide, as well as other reactive species are major factors involved in ischemia/reperfusion-induced liver injury.