Background and purpose: Damage caused by ischemia/reperfusion (I/R) is one of the major causes of liver failure during surgeries. Endothelin as the main vasoconstrictor has two receptors; ET_A and ET_B. Increased number of ET_B during ischemia-reperfusion, reduces tissue damages by sinusoidal dilation. This study investigated the effects of dexamethasone against liver endothelial glycocalyx injury and ET_B receptor gene expression during hepatic ischemia/reperfusion in rats.

Materials and methods: Thirty two male Wistar rats were divided into four groups; a SHAM-operated group that received normal saline, DEX; which had dexamethasone injection (10 mg/kg), the I/R; received normal saline during ischemia/reperfusion, and the DEX + IR with I/R that received dexamethasone (10 mg/kg, 60 minutes before ischemia and immediately after reperfusion). After 1 hour of ischemia and 3 hours of reperfusion the blood samples and liver tissues were collected. The relative gene expression of ET_B was assessed by real time PCR. Serum samples were used to measure the level of ALT and AST and hyaluronic acid (HA).

Results: The level of ALT, AST and HA significantly increased in I/R compared with those of the SHAM-operated group (P<0.001). Injection of dexamethasone in the DEX+IR caused a significant reduction in serum indicators compared to those of the I/R group (P<0.001). Elevated ET_B receptor gene expression reduced by dexamethasone injection (P> 0.05).

Conclusion: Dexamethasone decreased ET_B receptor gene expression during liver I/R. In addition, it significantly protected the parenchymal cells and sinusoidal endothelial glycocalyx. Therefore, dexamethasone could play an important role in reducing liver injury during I/R.