Background
Remote ischemic perconditioning (RIPER) has been already reported by our team to protect the liver from ischemic reperfusion injury (IRI) however the mechanism behind the positive effects of RIPER remains unrevealed. We aimed to investigate the potential role of neural elements to transfer protective signals evoked by perconditioning.

Materials and Methods
Male Wistar rats were randomly allocated into six groups (Sham, IR, RIPER with or without denervation; n=7/group). Half of the animals underwent left femoral and sciatic nerve resection. Twenty minutes recovery was allowed. In IR and RIPER groups, normothermic, 60 minutes long partial (70%) liver ischemia was induced, parallel animals in RIPER groups received perconditioning treatment (4x5-5min IR, left femoral clamping). Hepatic microcirculation (laser- Doppler-flowmetry) and blood pressure were monitored during the first post-ischemic hour. After 24h reperfusion liver samples were taken for histology and for the detailed analysis of redox-state alterations. Automated image analysis software was used for necrosis-quantification (Fraunhofer-Mevis). Serum ALT, AST levels were measured.

Result
Microcirculation and blood pressure showed significant improvement during reperfusion with perconditioning which phenomenon was completely abolished by nerve resection (p<0.05; RIPER vs. IR, IR+denervation, RIPER+denervation). Results of necrosis-quantification showed similar pattern (p<0.01; RIPER vs. IR, IR+denervation and RIPER+denervation; 6.6±2.5 vs. 37.9±3.1, 29.8±6.4, 34.7±4.7 respectively). Besides non-characteristic changes of the AST levels, ALT values were significantly lower (p<0.05) in RIPER group when compared to the other IRI groups. Further supporting results were obtained from the analysis of redox- homeostasis.

Conclusion
Perconditioning could reduce liver IRI in our model via a mechanism which most probably involves inter organ neural pathways.