Functional Assessment of Cardiac Arrest Hepatocytes and Effect of Mechanical Perfusion on Function in a Rat Model

Hepatocyte transplantation has been reported to be useful for metabolic diseases and acute liver failure. However, the shortage of donors limits its widespread use. The use of livers from donors after circulatory death, which are currently unavailable for liver transplantation, may alleviate donor shortage. In this study, we investigated the effects of mechanical perfusion on cardiac arrest hepatocytes in a rat model using cardiac arrest donor livers, and we evaluated the function of cardiac arrest hepatocytes.

F344 rat hepatocytes isolated from livers removed during cardiac pulsation were compared with those isolated from livers removed after 30 minutes of warm ischemia after cardiac arrest. We then compared hepatocytes isolated from livers removed after 30 minutes of warm ischemia with those isolated after 30 minutes of mechanical perfusion before isolation. The yield per liver weight, ammonia removal capacity, and adenosine diphosphate/adenosine triphosphate ratio were evaluated.

Thirty minutes of warm inhibition reduced hepatocyte yield but did not alter ammonia removal capacity and energy status. Mechanical perfusion increased hepatocyte yield and improved the adenosine diphosphate/adenosine triphosphate ratio after 30 minutes of warm inhibition.

Thirty minutes of warm ischemic time may decrease isolated hepatocyte yield without degrading their function. If increased yields are obtained, livers from donors dying of cardiac arrest could be used for hepatocyte transplantation. The results also suggest that mechanical perfusion may positively affect the energy status of hepatocytes.