Cytoprotective Effect of Somatostatin in A Rat Model of Hepatic Ischemic Reperfusion

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Abstract
To evaluate the possible cytoprotective effect of somatostatin in hepatic ischemic reperfusion injury we used 75 adult male Wistar rats randomly separated into four groups. The rats in group 1 underwent sham operations, and those in group 2 underwent resection of the median and left lateral lobes. The rats in group 3 underwent a 90–min period of ischemia of the right lateral lobe, which we induced by temporarily occluding the right portal vein and the hepatic artery. On restoration of flow to the right lateral lobe, the median and left lateral lobes (about 80% of total liver mass) were excised (and later assayed for thymidine kinase basal activity). The rats in group 4 were given the same treatment as group 3 rats except that a saline solution of somatostatin was infused at a rate of 2 μg/min starting at laparotomy and lasting 24 hr. The rats in groups 1, 2 and 3 were infused with saline. Rats in groups 2, 3 and 4 were randomly assigned to two subgroups; one of these subgroups was observed until spontaneous death, and rats in the other group were killed 24 hr after the procedure for obtaining peripheral blood and liver samples. Somatostatin infusion improved the animals' survival rates from 0% (group 3) to 60% (group 4) (p < 0.05) and decreased bilirubin levels (0.78 ± 0.17 mg/dl, n = 15 [group 4] vs. 1.69 ± 0.04 mg/dl, n = 15 [group 3]; p < 0.05). Hepatectomy alone (group 2) increased thymidine kinase activity from a basal level of 164.4 ± 6.9 pmol/mg to a level of 253.6 ± 7.6 pmol/mg of protein after 24 hr (n = 10, p < 0.001). In ischemic reperfusion groups (3 and 4) thymidine kinase activity was not modified. Our results suggest a cytoprotective effect for somatostatin. Although the exact mechanism of this action at the cellular level is unknown, it seems to be unrelated to an early increment in hepatocyte regeneration.