Abstract
To investigate the effects of intravenous L-arginine (LG) infusion on liver morphology, function and proinflammatory response of cytokines during the early phase of ischemia-reperfusion injury (IRI). Thirty rabbits were subjected to 60 minutes of hepatic ischemia and 120 minutes of reperfusion. An intravenous injection of saline or L-arginine was administered five minutes before the ischemia and five minutes before initiating the reperfusion and at the 55th and 115th minutes after the ischemia. Samples were collected for histological analysis of the liver and measurements of the serum AST, ALT and LDH and the cytokines IL-6 and TNF-alpha. It was observed a significant reduction of sinusoidal congestion, cytoplasmic vacuolization, infiltration of polymorphonuclear leukocyte, nuclear pyknosis, necrosis and steatosis in liver tissue, as well as AST, ALT and LDH after injection of LG in the ischemia (p <0.001). Lower levels of IL-6 and TNF-alpha were associated with LG infusion during ischemia. Higher levels these proteins were observed in animals receiving LG during reperfusion. L-arginine protects the liver against ischemia/reperfusion injury, mainly when is administered during the ischemic phase.
Highlights
MethodsIschemia-reperfusion injury (IRI) is associated with multiple events that affect liver function following transient episodes of hepatic ischemia, such as solid organ transplantation, trauma, hypovolemic shock, and elective liver resection, when inflow occlusion or total vascular exclusion is used to minimize blood loss[1]
One of the earliest events associated with the reperfusion of an ischemic liver is endothelial dysfunction that is characterized by a decreased production of endothelial cell-derived nitric oxide[3]
The greatest reductions in areas of sinusoidal congestion, cytoplasmic vacuolation, infiltrating polymorphonuclear leukocytes (PMNLs), nuclear pyknosis, hepatocyte necrosis, and steatosis were observed in the ischemia plus LG (I-LG) group followed sequentially by the ischemia and reperfusion plus LG (IR-LG) group, the ischemia plus saline (I-SS) group and the ischemia and reperfusion plus saline (IR-SS) group (Table 1)
Summary
MethodsIschemia-reperfusion injury (IRI) is associated with multiple events that affect liver function following transient episodes of hepatic ischemia, such as solid organ transplantation, trauma, hypovolemic shock, and elective liver resection, when inflow occlusion or total vascular exclusion is used to minimize blood loss[1]. One of the earliest events associated with the reperfusion of an ischemic liver is endothelial dysfunction that is characterized by a decreased production of endothelial cell-derived nitric oxide (eNO)[3]. This rapid post-ischemic decrease in NO bioavailability appears to be due to a decrease in the synthesis of NO, enhanced inactivation of NO via the overproduction of superoxide, or both phenomena[3,4]. High tissue levels of NO may have harmful effects[12,13,14,15,16] These observations suggest a balance between the local NO concentration and the time of NO exposure in determining the outcome of liver IRI8. Irrespective of the precise mechanisms involved, increased inflammation and cytotoxicity are key components in hepatocellular dysfunction during the pathogenesis of liver IRI16-20
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