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. 2019 Apr;51(3):919-924.
doi: 10.1016/j.transproceed.2018.12.028. Epub 2019 Jan 9.

Simulating Transplant Small-for-size Grafts Using Human Liver Monosegments: The Impact of Portal Perfusion Pressure

M Mohamed  1 , L Kang  1 , C Zhang  1 , B Edenfield  2 , J Sykes  1 , T Brown  3 , J L Johnson  3 , F Rehman  4 , J H Nguyen  5
Affiliations

Simulating Transplant Small-for-size Grafts Using Human Liver Monosegments: The Impact of Portal Perfusion Pressure

M Mohamed et al. Transplant Proc. 2019 Apr.

Abstract

Small-for-size-liver grafts (SFSG) in adult transplant recipients have elevated risk of graft failure, limiting its application in clinical liver transplantation. Relevant preclinical model of SFSG is lacking. Relevant to deceased-donor split liver transplant and living-donor liver transplant in adult recipients, in this study, we present our initial characterization of SFSG model using monosegments of a discarded human donor liver.

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Figures

Fig 1.
Fig 1.
Hemodynamic parameters of the monosegmental livers at varying portal perfusion pressures. (A) Segments II and IV were individually perfused in a LifePort system with William’s medium E plus GlutamaxAX; (B) Record tracing of portal perfusing pressures at baseline, 10, 20, and 30 mm Hg; (C) Hepatic flow at baseline and at increasing portal perfusion pressures; (D) Resistive indices of the monosegmental livers at varying portal perfusion pressures; (E) pH, partial pressures of oxygen and CO2, bicarbonate, oxygen saturation, glucose, and electrolytes were measured with an iSTAT CG8+ cartridge.
Fig 2.
Fig 2.
Histoimmunopathologic characterization of liver segments II and IV that were pretreated with GABA and vehicle, respectively, prior to oxygenated reperfusion at baseline and increasing portal perfusion pressures. Liver specimens taken at each time point from each liver segment were stained with hematoxylin and eosin for overall histologic evaluation, for CD31 for sinusoidal endothelial cells (ie, sinusoidal integrity), for Ki67 assessing proliferative activity, for TUNEL assessing apoptotic hepatocellular death, and for factor V assessing hepatocellular synthetic capacity.
Fig 3.
Fig 3.
Quantitative measurement of mRNA expression of CDKN1A/p21 with quantitative RT-PCR. Compared to the vehicle-treated segmental IV liver, the pretreatment with GABA in segment II liver lowered the mRNA expression of CDKN1A following the oxygenated reperfusion of the liver at 10 mm Hg, but not at subsequent portal perfusion pressures.
Fig 4.
Fig 4.
In situ hybridization of hepatocellular mRNA expression of CDKN1A/p21 with RNAscope. Compared to the positive and negative controls, intracellular expression of CDKN1A is visualized in the liver of segment II but not in segment IV.
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