Protective effect of intraportal infusion of hypothermic hydrogen-rich saline solution on hepatic warm ischemia/reperfusion injury in rat model

The aim of the present study was to investigate the effects of intraportal administration of hypothermic hydrogenrich saline solution (HRSS) on hepatic ischemia/reperfusion (I/R) injury. Thirty rats were divided equally into six groups; 1) sham, no I/R or transfusion, 2) I/R injury (60 minutes ischemia + 120 minutes reperfusion, 3) I/R injury + normal saline 24C, 4) I/R injury + normal saline 4C, 5) I/R injury + HRSS 24C, 6) I/R injury + HRSS 4C. In groups 3-6, 1 mg/kg normal saline (NS) and/or HRSS were administered into the vein of the left lateral and median lobes of the liver (upper the site of clumping) 10 minutes before finishing of ischemic period. The harvest time points were at 2 hours post reperfusion in all groups. Cell death, sinusoidal dilatation, congestion, hemorrhage, and neutrophil infiltration were observed in I/R group, while these histopathological changes were attenuated in the hypothermic HRSS administrated groups (P < 0.01). The level of alanine aminotransferase, aspartate aminotransferase, malondialdehyde, interleukin 6, tumor necrosis factor a, and caspase-3 were increased significantly by I/R injury and hypothermic HRSS administration reduced all these markers (P < 0.01). SOD level was low in I/R group whereas it tended to increase in the hypothermic HRSS administrated groups (P < 0.01). The present study demonstrated that hypothermic hydrogen-rich saline solution effectively protected the hepatic tissue against cellular injury and organ dysfunction through the mechanisms that decrease the effect of oxidative stress, inflammation, apoptosis and necrosis.(AU)

Protective effect of intraportal infusion of hypothermic hydrogen-rich saline solution on hepatic warm ischemia/reperfusion injury in rat model

The aim of the present study was to investigate the effects of intraportal administration of hypothermic hydrogenrich saline solution (HRSS) on hepatic ischemia/reperfusion (I/R) injury. Thirty rats were divided equally into six groups; 1) sham, no I/R or transfusion, 2) I/R injury (60 minutes ischemia + 120 minutes reperfusion, 3) I/R injury + normal saline 24C, 4) I/R injury + normal saline 4C, 5) I/R injury + HRSS 24C, 6) I/R injury + HRSS 4C. In groups 3-6, 1 mg/kg normal saline (NS) and/or HRSS were administered into the vein of the left lateral and median lobes of the liver (upper the site of clumping) 10 minutes before finishing of ischemic period. The harvest time points were at 2 hours post reperfusion in all groups. Cell death, sinusoidal dilatation, congestion, hemorrhage, and neutrophil infiltration were observed in I/R group, while these histopathological changes were attenuated in the hypothermic HRSS administrated groups (P < 0.01). The level of alanine aminotransferase, aspartate aminotransferase, malondialdehyde, interleukin 6, tumor necrosis factor a, and caspase-3 were increased significantly by I/R injury and hypothermic HRSS administration reduced all these markers (P < 0.01). SOD level was low in I/R group whereas it tended to increase in the hypothermic HRSS administrated groups (P < 0.01). The present study demonstrated that hypothermic hydrogen-rich saline solution effectively protected the hepatic tissue against cellular injury and organ dysfunction through the mechanisms that decrease the effect of oxidative stress, inflammation, apoptosis and necrosis.