Abstract
It was reported that prevention of acute portal overpressure in small-for-size livers by inflow modulation results in a better postoperative outcome. The aim is to investigate the impact of portal blood flow reduction by splenic artery ligation after major hepatectomy in a murine model. Forty-eight rats were subjected to an 85% hepatectomy or 85% hepatectomy and splenic artery ligation. Both groups were evaluated at 24, 48, 72 and 120 post-operative hours: liver function, regeneration and viability. All methods and experiments were carried out in accordance with Coimbra University guidelines. Splenic artery ligation produces viability increase after 24 h, induces a relative decrease in oxidative stress during the first 48 hours, allows antioxidant capacity increment after 24 h, which is reflected in a decrease of half-time normalized liver curve at 48 h and at 72 h and in an increase of mitotic index between 48 h and 72 h. Splenic artery ligation combined with 85% hepatectomy in a murine model, allows portal inflow modulation, promoting an increase in hepatocellular viability and regeneration, without impairing the function, probably by inducing a less marked elevation of oxidative stress at first 48 hours.
Highlights
Several reports suggest that postoperative liver failure is due to reduced liver volume and posthepatectomy hemodynamic changes, that induce production of reactive oxygen species (ROS) and inflammatory cytokines, leading to hepatic necrosis and apoptosis[1,2,9,10]
For these reasons we propose to perform a wider research on the impact of splenic artery ligation, as a technically feasible manoeuver to modulate the portal inflow after major hepatectomy in a murine model, assessing their effects on hepatocellular function, regeneration and viability
The results of this study showed that splenic artery ligation produced significant viability increase at 24 h which remained over time, inducing a decrease in intracellular accumulation of peroxides and superoxide radical during the first 48 hours
Summary
Several reports suggest that postoperative liver failure is due to reduced liver volume and posthepatectomy hemodynamic changes, that induce production of reactive oxygen species (ROS) and inflammatory cytokines, leading to hepatic necrosis and apoptosis[1,2,9,10]. Pharmacological trials and surgical techniques have been tested, individually but as a complement, namely somatostatin and analogues[14,15,16], prostaglandin E117,18, FK 409 and FTY 72019,20, terlipressin[21], inhalation of nitric oxide, carbon monoxide and hydrogen[22,23,24], portal caval shunt[25,26] or other portal derivative manoeuvres to prevent its excessive shunting and frequent complications[27,28], plasmapheresis and other plasma purification procedures in order to decrease serum toxin levels[29,30] None of these strategies resulted in a significant survival increase because they have shown an inhibitory effect on liver regeneration after hepatectomy, which limits their use in hepatic surgery[31]. The first work confines itself to study the injurious effects on liver parenchyma, cell regeneration and survival, while the second one tested the protective effect of the splenic artery ligation through induction of heme oxygenase-1 (HO-1) expression
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