Sevoflurane prevents liver inflammatory response induced by lung ischemia-reperfusion.

Abstract

Background: Transplants cause ischemia-reperfusion (IR) injury that can affect distant organs. Liver is particularly sensitive to IR injury. The present randomized experimental study was designed to investigate a possible protective effect of sevoflurane against liver inflammatory response to lung IR in a lung upper lobe left autotransplant model.

Methods: Two groups (sevoflurane and control) of eight swines each were submitted to upper lobe left lung autotransplant. Hypnotic maintenance was performed with sevoflurane 3% or propofol 8 to 10 mg/kg per hr until pneumonectomy was done; then propofol was used for all animals. Blood and liver samples were taken in four different moments: prepneumonectomy, prereperfusion, 10 min postreperfusion and 30 min postreperfusion to measure levels of interleukin (IL)-1β, IL-10, tumor necrosis factor (TNF)-α, monocyte chemotactic protein (MCP)-1, nuclear factor (NF)-κB, C-reactive protein, ferritin and caspase 3. Non-parametric test was used to find statistical meaning.

Results: Lung IR markedly increased the expression of TNF-α, IL-1β, MCP-1, NF-κB and caspase activity in control livers compared with basal levels, whereas liver IL-10 expression decreased 10 and 30 min post-reperfusion. Sevoflurane significantly decreased TNF-α, IL-1β, MCP-1, NF-κB liver expression and caspase 3 activity. Sevoflurane also reverted the lung IR-induced decrease in IL-10 expression.

Conclusions: The present results indicate that lung IR caused hepatic injury. Sevoflurane attenuated liver injury in a model of upper lobe left lung autotransplant in pigs.