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.
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