Prostaglandins of the E series have been shown to decrease renal and hepatic ischemic injury as well as improve hepatic function in patients with primary non-function following transplantation. We wished to determine the effect of prostaglandin E1 (PGE1) on hepatic allograft reperfusion injury in the isolated perfused rat liver (IPRL) model. Livers were harvested from adult male Sprague-Dawley rats and the bile duct, portal vein, and suprahepatic vena cava were cannulated. Control livers were placed immediately on the IPRL apparatus and perfused for 2 hr with a blood-Kreb's solution. Group A and B allografts were stored for 8 hr in heparinized lactated Ringer's solution at 4°C. Group A livers were then perfused with a PGE1 infusion at 0.1 μg/kg/min while B livers received a placebo infusion of NS at the same rate. Temperature, pH, and inflow pressures were kept constant. Oxygen consumption, portal flow, and resistance were calculated for each group and found not to be statistically different. LDH, SGOT, superoxide anion (SOA), and bile flow were measured at 30-min intervals. At the end of the 2-hr perfusion, the placebo Group B (N = 5) had LDH, SGOT, and SOA higher than those of either Group A (N = 5) or control (N = 4) livers. The difference between Group A and Group B was significant for SGOT and SOA (P < 0.05). Bile flow was highest in the control group (24.2 ± 1.8 μl/g/30 min). Group A livers produced bile at a similar rate (19.1 ± 2.5 μl/g/30 min), while Group B bile rate was markedly reduced (11.2 ± 2.5 μl/g/30 min). The difference between Groups A and B was not significant (P = 0.06). Histologically, allografts in Group B demonstrated cellular edema and pale staining while those in Group A showed normal hepatic architecture with no evidence of injury, comparable to those of control livers. In conclusion, PGE1 infusion reduces hepatic injury following extended cold storage and reperfusion as determined by decreased SGOT, SOA, and preservation of hepatic architecture.
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