Remote preconditioning improves hepatic oxygenation after ischaemia reperfusion injury

Hepatic ischaemia reperfusion injury (IRI) lowers hepatic oxygenation and induces tissue acidosis. Remote ischaemic preconditioning (RIPC) reduces hepatic IRI through increased hepatic blood flow but its effect on hepatic oxygenation and acidosis is not known. This study investigates these effects through near infrared spectroscopy (NIRS). Twenty-four NZ rabbits were grouped into four: sham, RIPC, IRI alone, RIPC + IRI. RIPC was induced through three cycles of 10 min ischaemia and reperfusion to the limb. Total hepatic ischaemia was produced by complete portal inflow occlusion for 25 min. Serum transaminases, bicarbonate and hepatic venous nitrite/nitrate (NOx) levels were measured 2 h postreperfusion. Hepatic oxygenation was monitored with NIRS. At 2 h post reperfusion, IRI alone resulted in reduced mitochondrial oxygenation (CytOx CuA Redox), serum bicarbonate, hepatic venous NOx with an increase in serum transaminases and hepatic deoxyhaemoglobin levels. RIPC before IRI caused significant improvement in mitochondrial oxygenation (P = 0.01), increased serum bicarbonate (P = 0.02), hepatic venous NOx (P = 0.025) with a decrease in serum transaminases (P = 0.04) and hepatic deoxyhaemoglobin levels (P = 0.03). There was a positive correlation (P = 0.02) between hepatic venous NOx levels and mitochondrial oxygenation. RIPC before IRI improves hepatic mitochondrial oxygenation and reduces acidosis and currently undergoing clinical study.