Background. Pharmacological preconditioning is one of the tools used to diminish preservation injury. We investigated the influence of sevoflurane preconditioning of liver grafts on postoperative graft function. Methods. Consecutive 60 deceased brain donors were randomized into sevoflurane group or control group. In sevoflurane group donors were treated with endexpiratory 2,0 volume% of sevoflurane during procurement. Primary endpoint was postoperative liver injury. Secondary endpoint was incidence of early allograft dysfunction (EAD). Results. The groups were not different in median DRI, donor age, graft steatosis, and MELD score. Peak AST and ALT levels were lower in sevoflurane group than in control group: 792 and 1861 (P = 0, 038) for AST and 606 and 1191 for ALT (P = 0, 117). Incidence of EAD was 16,7% in sevoflurane group and 50% in control group (Fisher test, P = 0, 013). In subgroups without steatosis preconditioning with sevoflurane did not have influence on incidence of EAD. In subgroups with mild and moderate steatosis incidence of EAD was lower in recipients of liver grafts treated with sevoflurane. Conclusions. Preconditioning with sevoflurane during organ procurement improves graft function by lowering incidence of early allograft dysfunction, particularly in recipients of steatotic liver grafts.
It was shown that Tacrolimus (TAC) can suppress inflammation and immune response involved in liver ischemic reperfusion injury (IRI) (Kristo I., Transpl Int. 2011). The aim: We hypothesize that back-table arterial and portal liver perfusion with TAC can influence the incidence and severity of EAD. A prospective randomized study was conducted (ClinicalTrials.gov Identifier: NCT01887171). Materials and methods: Including criteria: 1 st liver transplantation from DBD donor with sequential portal-arterial reperfusion. At back-table portal vein and hepatic artery were perfused each by 500 ml of HTK solution containing 20 ng/ml TAC during 10-15 min followed by portal flushing with 200 ml 5% solution of Albumin containing 20 ng/ml TAC and by resting of liver in effluent. No Tac was added in the control group. Primary Outcome: EAD (Olthoff KM, et al. Liver Transpl. 2010) and severe EAD (P.R. Salvalaggio, et al. Transpl. Proceedings, 2012). Results: No difference was found between groups (main vs. control) in terms of MELD (16 vs. 16), steatosis (10 vs. 10%), ballooning (45 vs. 40%) of liver grafts, recipient's age (50 vs. 50y), warm ischemia time (50 vs. 50 min) and total ischemia time (482.5 vs. 485.0 min). Median donor age was higher in the main group (44.5 vs. 39.0y). The overall rate of EAD was 27.9%. EAD rate was significantly lower in the main group (6/43 vs. 18/43; p=0.003). The rate of moderate-to-severe EAD was lower in the main group (1/43 vs. 10/43; p=0.009). The median level of AST and ALT 24 h after reperfusion were significantly lower in the intervention group (1004 vs. 1596; p=0.03 and 449 vs. 759; p=0.057). Conclusion: Portal and arterial back-table liver perfusion by HTK solution with Tacrolimus may contribute to lower EAD incidence and severity.
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