Liver injury following normothermic ischemia in steatotic rat liver

Authors

  • Ai-Min Hui,

    1. First Department of Surgery, Shinshu University School of Medicine, Shinshu University Hospital, 3–1–1 Asahi, Matsumoto 390, Japan
    Search for more papers by this author
  • Seiji Kawasaki,

    1. First Department of Surgery, Shinshu University School of Medicine, Shinshu University Hospital, 3–1–1 Asahi, Matsumoto 390, Japan
    Search for more papers by this author
  • Dr. Masatoshi Makuuchi,

    Corresponding author
    1. First Department of Surgery, Shinshu University School of Medicine, Shinshu University Hospital, 3–1–1 Asahi, Matsumoto 390, Japan
    • Professor and Chairman, First Department of Surgery, Shinshu University School of Medicine, 3–1–1 Asahi, Matsumoto 390, Japan
    Search for more papers by this author
  • Jun Nakayama,

    1. Central Clinical Laboratories, Shinshu University Hospital, 3–1–1 Asahi, Matsumoto 390, Japan
    Search for more papers by this author
  • Toshihiko Ikegami,

    1. First Department of Surgery, Shinshu University School of Medicine, Shinshu University Hospital, 3–1–1 Asahi, Matsumoto 390, Japan
    Search for more papers by this author
  • Shinichi Miyagawa

    1. First Department of Surgery, Shinshu University School of Medicine, Shinshu University Hospital, 3–1–1 Asahi, Matsumoto 390, Japan
    Search for more papers by this author

Abstract

The influence of normothermic ischemia on steatotic liver was compared with that on healthy liver in rats. Steatotic liver was induced with 4 wk of a cholinedeficient diet. We used a procedure of subcutaneous spleen transposition to develop portosystemic collaterals to avoid splanchnic stasis during total hepatic vascular occlusion. One-week survival rates after 30, 45, and 60 min of normothermic ischemia were 75%, 20% and 0% in the steatotic liver group and 100%, 90% and 70% in the control group, respectively. Significantly poor restoration of energy metabolism was observed in the steatotic liver group. After 1 hr of reflow following 45 and 60 min of ischemia, ATP was restored to 74% and 50%, respectively, of the preischemic level in healthy liver but to only 44% and 27% respectively, in steatotic liver. Microscopically, focal hemorrhage, disruption of the sinusoidal microvasculature and occasional spotty necrosis of hepatocytes were demonstrated after 1 hr of reflow following ischemia in steatotic liver, but no significant changes were evident in healthy liver. This microcirculatory alteration seems to be responsible for the loss of organ viability in steatotic liver. We suggest that steatotic liver is more vulnerable than healthy liver to normothermic ischemia in the rat. (Hepatology 1994;20:1287–1293).

Ancillary