IN-VIVO DEMONSTRATION OF IMPAIRED MICROCIRCULATION IN STEATOTIC HUMANLIVER GRAFTS

Citation
Am. Seifalian et al., IN-VIVO DEMONSTRATION OF IMPAIRED MICROCIRCULATION IN STEATOTIC HUMANLIVER GRAFTS, Liver transplantation and surgery, 4(1), 1998, pp. 71-77
Citations number
37
Categorie Soggetti
Gastroenterology & Hepatology",Surgery,Transplantation
ISSN journal
10743022
Volume
4
Issue
1
Year of publication
1998
Pages
71 - 77
Database
ISI
SICI code
1074-3022(1998)4:1<71:IDOIMI>2.0.ZU;2-B
Abstract
The perfusion of human donor livers was studied during organ retrieval using laser Doppler flowmetry to assess the microcirculatory alterati on caused by fatty infiltration (steatosis). Using a multichannel lase r Doppler flowmeter, we measured the hepatic perfusion as flux units i n 21 liver donors, eight of which were macroscopically fatty. Perfusio n was recorded continuously for 2 minutes from two sites on each lobe at the beginning of organ retrieval, after the vascular dissection, an d during sequential occlusion of the hepatic artery and portal vein. M ean flux value and SEM were calculated, and paired Student's t test wa s used for comparison between stages of perfusion. Multiple ANOVA was used to determine whether factors other than the normal or fatty paren chyma influenced the perfusion measurements. Mobilization of the graft did not affect parenchymal perfusion. Perfusion was significantly (P < 0.001) and rapidly reduced with hepatic artery or portal vein occlus ion in both groups. Macroscopically steatotic livers (n = 8) had dimin ished microcirculation compared with normal livers (n = 13) (125 +/- 1 8 v 252 +/- 24 flux units; P = 0.002). Donors receiving inotropes (n = 10) had a lower mean perfusion rate (150 +/- 20 v 252 +/- 29 flux uni ts; P = 0.026), but this effect was found in both the normal and steat otic groups with no interaction (ANOVA; P = 0.658). Steatosis diminish es the tissue perfusion in human liver grafts. Laser Doppler flowmetry may help identify grafts with a compromised microcirculation. Copyrig ht (C) 1998 by the American Association for the Study of Liver Disease s.