Preconditioning with
noble gases serves as an effective strategy to diminish tissue injury in different organs. The aim of this study was to investigate the influence of pretreatment with the nonanesthetic noble gas
helium on hepatic injury after
warm ischemia and reperfusion (IR) in comparison to ischemic preconditioning (IPC). Anesthetized and ventilated rats were randomized into six groups (n = 8/group):
sham: after
laparotomy, the portal triad was exposed without clamping; IPC was performed with 10 min of partial liver
ischemia and 10 min of reperfusion; HePC: three cycles of 5 min with inhalation of
helium 70 vol% and intermittent washout;
IR: 45 min of
ischemia followed by 240 min of reperfusion; IPC-IR: IPC followed by hepatic IR; HePC-IR: pretreatment with
helium 70 vol% followed by hepatic IR. Hepatic injury was evaluated by measurement of serum
enzymes aspartate aminotransferase and
alanine aminotransferase. Hepatic
mRNA expression and serum levels of
tumor necrosis factor α (TNF-α) and
interleukin 10 (IL-10) were measured with real-time quantitative polymerase chain reaction and
enzyme-linked
immunosorbent assay, respectively.
Myeloperoxidase in liver tissue was assessed spectrophotometrically as a marker of neutrophil accumulation.
mRNA levels of
heme oxygenase 1 in liver tissue were assessed to investigate a
protein of the most abundant protective system in the liver.
Aspartate aminotransferase and
alanine aminotransferase serum activities increased after hepatic IR (
sham vs. IR; P < 0.05). The serum levels of liver
enzymes after IR were significantly diminished with IPC (P < 0.05), whereas
helium pretreatment had no effect.
mRNA expression of TNF-α increased in all groups except IPC-IR compared with
sham, whereas
mRNA expression of
IL-10 increased only after
helium pretreatment. Serum levels of
IL-10 were not affected by any intervention, whereas serum levels of TNF-α and liver
myeloperoxidase were increased after IR, but not after HePC-IR. In conclusion, pretreatment with inhaled
helium does not attenuate hepatic injury after warm IR of the liver, although there is evidence for a modulation of the inflammatory response.