Reperfusion injury represents a key event leading to graft nonfunction. Maintaining adequate
nitric oxide levels and stimulating
vasodilator synthesis can probably minimize endothelial damage. The aim of this study was to investigate the effect of
L-arginine, a substrate of
nitric oxide synthesis, and
oligotide, a promoter of
prostacyclin synthesis, on liver function and morphology after
warm ischemia-
reperfusion injury. After constructing a side-to-side
portacaval shunt,
ischemia was induced by clamping the hepatic hilum for 2 h above the shunt, in 19 female pigs divided into a control group (n = 7), an
L-arginine treatment group (n = 6), and an
oligotide treatment group (n = 6). Liver function tests and measurements of serum and red blood cell
malondialdehyde and plasma
nitric oxide levels were performed before reperfusion and at 1, 10, 60, and 120 min after reperfusion. Liver biopsies, taken before reperfusion and at 30 min and 7 days after reperfusion, were analyzed for tissue
malondialdehyde, histological-ultrastructural features, and apoptosis evaluation. Thirty minutes after reperfusion, liver
malondialdehyde, sinusoidal congestion,
necrosis, and apoptosis were significantly lower in the
L-arginine group than in the controls (p < .05). On postoperative day 7, tissue
malondialdehyde decreased, while plasma
nitric oxide and hepatocyte
glycogen content were increased in the
L-arginine group compared to controls (p < .05). This study demonstrates the protective effect of
L-arginine on hepatic lipoperoxidation and liver morphology in a pig model of
warm ischemia-
reperfusion injury. The increased plasma levels of
nitric oxide a week after
ischemia-reperfusion injury support the hypothesis that it has a role in preventing liver damage. The same beneficial effect was not confirmed for
oligotide.