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Updated: Jul 3, 2026
Heterotopic Auxiliary Rat Liver Transplantation With Flow-regulated Portal Vein Arterialization in Acute Hepatic Failure
Published on: September 13, 2014
Urinary trypsin inhibitor improves viability of the liver in brain-dead rats
Koichi Itabashi1, Kazunori Furuta, Tsuyoshi Takahashi
1Department of Surgery, Kitasato University School of Medicine, 1-15-1 Kitasato, Sagamihara, Kanagawa 228-8555, Japan. itako@kitasato-u.ac.jp
Background/Aims:
The present study examined the effect of urinary trypsin inhibitor (UTI) on liver injury in hypotensive brain-dead rats.
Methods:
Brain death was induced by inflating a balloon catheter placed in the epidural space. UTI (100,000 units/kg/hour) was intravenously administered from 30 min until 6 hours after the induction of brain death. Systemic hemodynamics and hepatic tissue flow (HTF) were measured, and blood samples and hepatic tissue specimens for morphological examinations were obtained during the experiments.
Results:
The induction of brain death caused a 30% decrease in both mean arterial pressure and HTF, and an increase in the serum transaminase level in comparison with sham-operated rats. Brain death also increased the serum concentration of cytokine-induced neutrophil chemoattractant (CINC) (4.4-fold), as well as the number of CINC-positive cells (4.4-fold) and sequestered neutrophils in the sinusoids (3.1-fold). Post-treatment of brain-dead rats with UTI restored the HTF and reduced serum transaminase level. UTI decreased plasma CINC level and the number of neutrophils and CINC-positive cells in the sinusoids.
Conclusions:
The results suggest that treatment with UTI after the establishment of brain death improved the viability of the liver in hypotensive brain-dead rats by inhibiting CINC production.
