The effects of prostaglandin E₁ and tyrosine kinase inhibitors on energy status and protein synthetic ability in hepatic ischemia-reperfusion injury

The effects of prostaglandin E₁ (PGE₁) and tyrosine kinase inhibitors on hepatic energy status and protein synthesis in ischemic livers were studied using ³¹P-magnetic resonance spectroscopy in a rat model. The continuous administration of PGE₁ significantly increased the β-adenosine triphosphate/inorganic phosphate (β-ATP/P₁) ratio and hepatic protein synthesis rate (HPS) after ischemia-reperfusion injury. Microscopic examination showed that the continuous administration of PGE₁ inhibited the development of sinusoidal hemorrhage and edema. Thus, it was concluded that PGE₁ has a beneficial effect on ischemia-reperfusion injury in the liver. Pretreatment with tyrosine kinase inhibitor also increased the β-ATP/P₁ ratio; however, when tyrosine kinase inhibitor was injected before ischemia, the HPS became significantly reduced. Based on these data, the protective effect of tyrosine kinase inhibitor is unconvincing.