Prostaglandin E1 reduces thromboxane A2 in hepatic ischemia-reperfusion

Prostaglandin E1 is well documented to exert cytoprotective effects in ischemia-reperfusion injury in the liver. This study was designed to evaluate the changes in prostanoid concentrations and to delineate the mechanism of the cytoprotective effect of prostaglandin E1 in hepatic ischemia-reperfusion injury.

Mongrel dogs were divided into 3 groups: a control group, an ischemia-reperfusion group (I-R group), and a group that received prostaglandin E1 and was then subjected to ischemia-reperfusion. Liver ischemia was produced for 60 min using the Pringle maneuver. The concentrations of aspartate aminotransferase, alanine aminotransferase, prostaglandin I2, thromboxane A2, and lipid peroxides in hepatic venous blood were examined before and after the Pringle maneuver in the latter 2 groups, and at the corresponding points in the control group.

In the I-R group, aspartate aminotransferase and alanine aminotransferase after ischemia-reperfusion were significantly higher than those in the control group, and these values also rose significantly after ischemia-reperfusion in the prostaglandin E1-treated group. However, prostaglandin E1 administration suppressed significantly the increase compared with the I-R group. In the I-R group, prostaglandin I2, thromboxane A2, and lipid peroxide production in the liver increased 5 min after unclamping. The increases in thromboxane A2 and lipid peroxide production before and after ischemia-reperfusion were decreased, and prostaglandin I2 production was increased before ischemia-reperfusion in the group that was pretreated with prostaglandin E1.

Prostaglandin E1 is involved protecting against warm ischemic liver damage by not only suppressing the increased thromboxane A2 production, but also by increasing prostaglandin I2 production.