title: Prostaglandin E(1) continuous hepatic arterial infusion in the treatment of postoperative acute liver failure: basic study on hepatic hemodynamics and clinical application.
abstract: OBJECTIVE
  In the treatment of severe liver damage, it is of greater advantage to administer prostaglandin E(1) (PGE(1)) directly to the liver compared with systemic intravenous infusion, because of its high inactivation rate in the lungs. In comparison with intraportal infusion, hepatic arterial infusion is more advantageous because of its easier and safer accessibility. This study was designed to prove the superiority of hepatic arterial infusion to intravenous infusion.
  
  
  METHODS
  Changes in hepatic hemodynamics and oxygen delivery accompanying PGE(1) infusion using both methods were investigated in pigs. In addition, continuous hepatic arterial infusion was applied in 3 cases of postoperative acute liver failure, for patients in whom other conventional treatments like plasma exchange failed to improve the functioning of the liver.
  
  
  RESULTS
  Hepatic arterial flow increased significantly accompanying hepatic arterial infusion of PGE(1) at a rate of 0.1 microg/kg/min compared with intravenous infusion at the same rate in pigs. Such an increase resulted in elevation of total hepatic blood flow and oxygen delivery to the liver. Correspondingly, bile flow significantly increased accompanying hepatic arterial infusion of PGE(1). Continuous hepatic arterial infusion was applied in 3 cases of postoperative acute liver failure. The infusion was continued for 7-9 days at a rate of 0.01 microg/kg/min without any complications through heparin-coated catheters inserted via the femoral artery. Significant increase in bile flow was observed in 2 cases in whom bile was collected, serum total bilirubin began to decrease in all these 3 cases, and the patients recovered from acute liver failure.
  
  
  CONCLUSIONS
  Hepatic arterial infusion of PGE(1) is very useful and effective in the treatment of acute liver failure.
authors.affiliation: Department of Surgery, Akita University School of Medicine, Japan. sato@surg1.med.akita-u.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Sato
authors.forename: Y
authors.initials: Y
authors.lastname: Asanuma
authors.forename: T
authors.initials: T
authors.lastname: Kurokawa
authors.forename: T
authors.initials: T
authors.lastname: Kato
authors.forename: O
authors.initials: O
authors.lastname: Yasui
authors.forename: T
authors.initials: T
authors.lastname: Kusano
authors.forename: K
authors.initials: K
authors.lastname: Koyama
mesh_terms: D000368:Aged; D000527:Alprostadil / Q000008:administration & dosage* / Q000627:therapeutic use; D000818:Animals; D005260:Female; D006439:Hemodynamics; D006801:Humans; D007261:Infusions, Intra-Arterial; D007262:Infusions, Intravenous; D008099:Liver / Q000503:physiopathology*; D017114:Liver Failure, Acute / Q000188:drug therapy* / Q000503:physiopathology*; D008297:Male; D010100:Oxygen / Q000097:blood; D011169:Portal Vein; D012039:Regional Blood Flow; D013552:Swine; D014665:Vasodilator Agents / Q000008:administration & dosage* / Q000627:therapeutic use
chemical_list: D014665:Vasodilator Agents; D000527:Alprostadil; D010100:Oxygen