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Acute impairment of hepatic microcirculation and recruitment of nonparenchymal cells by intrasplenic hepatocyte transplantation.

Abstract：

BACKGROUND/PURPOSE:Over the last 20 years, hepatocyte transplantation (HcTx) has advanced from the experimental to the clinical stage. To date, HcTx has been performed in 30 patients in the United States. Regardless whether hepatocytes are transplanted into the spleen and migrate to the liver or are injected directly into the portal vein, transplanted liver cells will, to some extent, congest the recipient liver microcirculation. The potential negative consequences of intrasplenic HcTx were the subject of this study. METHODS:By using intravital microscopy, the authors investigated whether intrasplenic HcTx of 20 x 10(6) allogenic hepatocytes would influence liver perfusion, excretory liver function, and nonparenchymal cells (Kupffer and Ito cells) in vivo. RESULTS:The sinusoidal perfusion rate declined significantly from 94% (control) to 84% on day 1 and 76% on day 7. Bile acid excretion decreased in a similar fashion from 0.924 mg/h (control) to 0.669 mg/h on day 7. The authors observed a significant increase of Ito cells from 81.1 cells per microscopic field (control) to 97.1 (day 1) and an increase of Kupffer cells (KC; 6.1 cells per microscopic field on day 1 v 3.8 on control). CONCLUSIONS:This study shows an acute impairment of hepatic microcirculation and hepatucellular function along with an recruitment and activation of nonparenchymal cells in the early posttransplantation period after intrasplenic HcTx. Kupffer cell recruitment indicates an activation of local host defense, and Ito cell activation implies the initiation of liver repair mechanisms owing to ischemia-related cell damage.

journal_name

J Pediatr Surg

journal_title

Journal of pediatric surgery

authors

Wilhelm A,Leister I,Sabandal P,Krause P,Becker H,Markus PM

doi

10.1016/j.jpedsurg.2004.04.020

subject

Has Abstract

pub_date

2004-08-01 00:00:00

pages

1214-9

issue

8

eissn

0022-3468

issn

1531-5037

pii

S0022346804002714

journal_volume

39

pub_type

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