PGE1 reduces injury in hepatic allografts following preservation

Kim M. Olthoff, Evette Wasef, Philip Seu, David K. Imagawa, Julie A. Freischlag, John Hart, Ronald W. Busuttil

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Abstract

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.

Original languageEnglish (US)
Pages (from-to)595-601
Number of pages7
JournalJournal of Surgical Research
Volume50
Issue number6
DOIs
StatePublished - 1991

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Alprostadil
Allografts
Liver
Wounds and Injuries
Aspartate Aminotransferases
Bile
Superoxides
Placebos
Venae Cavae
Portal Vein
Prostaglandins E
Bile Ducts
Reperfusion Injury
Oxygen Consumption
Reperfusion
Sprague Dawley Rats

ASJC Scopus subject areas

  • Surgery

Cite this

Olthoff, K. M., Wasef, E., Seu, P., Imagawa, D. K., Freischlag, J. A., Hart, J., & Busuttil, R. W. (1991). PGE1 reduces injury in hepatic allografts following preservation. Journal of Surgical Research, 50(6), 595-601. https://doi.org/10.1016/0022-4804(91)90048-Q

PGE1 reduces injury in hepatic allografts following preservation. / Olthoff, Kim M.; Wasef, Evette; Seu, Philip; Imagawa, David K.; Freischlag, Julie A.; Hart, John; Busuttil, Ronald W.

In: Journal of Surgical Research, Vol. 50, No. 6, 1991, p. 595-601.

Research output: Contribution to journalArticle

Olthoff, KM, Wasef, E, Seu, P, Imagawa, DK, Freischlag, JA, Hart, J & Busuttil, RW 1991, 'PGE1 reduces injury in hepatic allografts following preservation', Journal of Surgical Research, vol. 50, no. 6, pp. 595-601. https://doi.org/10.1016/0022-4804(91)90048-Q
Olthoff KM, Wasef E, Seu P, Imagawa DK, Freischlag JA, Hart J et al. PGE1 reduces injury in hepatic allografts following preservation. Journal of Surgical Research. 1991;50(6):595-601. https://doi.org/10.1016/0022-4804(91)90048-Q
Olthoff, Kim M. ; Wasef, Evette ; Seu, Philip ; Imagawa, David K. ; Freischlag, Julie A. ; Hart, John ; Busuttil, Ronald W. / PGE1 reduces injury in hepatic allografts following preservation. In: Journal of Surgical Research. 1991 ; Vol. 50, No. 6. pp. 595-601.
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abstract = "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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T1 - PGE1 reduces injury in hepatic allografts following preservation

AU - Olthoff, Kim M.

AU - Wasef, Evette

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AU - Hart, John

AU - Busuttil, Ronald W.

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N2 - 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.

AB - 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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