Cold preservation of fatty liver grafts: prevention of functional and ultrastructural impairments by venous oxygen persufflation

Citation
T. Minor et al., Cold preservation of fatty liver grafts: prevention of functional and ultrastructural impairments by venous oxygen persufflation, J HEPATOL, 32(1), 2000, pp. 105-111
Citations number
29
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
JOURNAL OF HEPATOLOGY
ISSN journal
01688278 → ACNP
Volume
32
Issue
1
Year of publication
2000
Pages
105 - 111
Database
ISI
SICI code
0168-8278(200001)32:1<105:CPOFLG>2.0.ZU;2-P
Abstract
Background/Aims: The incidence of steatosis in livers retrieved for organ t ransplantation is up to 30%, Due to the shortage of donor organs, many of t hese livers are accepted for clinical transplantation, although a high rate of graft dysfunction is associated with ischemic preservation of steatotic livers. The present study was intended to reduce the ischemia/reperfusion injury of steatotic grafts by the use of venous systemic oxygen persufflati on during cold storage, Methods: A histologically-documented mild to moderate steatosis was induced in livers of Wistar rats by fasting for 2 days and subsequent feeding of a fat-free diet enriched in carbohydrates. Fatty livers were retrieved and f lushed via the portal vein with 60 mi of HTK. In group A, livers were then stored ischemically at 4 degrees C for 24 h, Livers of group B were additio nally connected to a gaseous oxygen supply and persufflated with O-2 via th e venous vascular system during the cold storage period, Viability of the l ivers was then assessed upon isolated perfusion in vitro with oxygenated Kr ebs-Henseleit buffer, Results: Venous systemic oxygen sufflation resulted in a relevant and signi ficant reduction of parenchymal (ALT: 132+/-90 vs 434+/-172 U/l; p<0.01) an d mitochondrial (GLDH: 116+/-57 vs 633+/-241 U/l; p<0.001) enzyme release d uring reperfusion. Moreover, Kupffer cell activation, as evaluated from aci d phosphatase activity in the perfusate, was reduced to about 1/3 (4.0+/-1. 3 vs 11.9+/-5.3 U/l; p<0.01). Electron microscopic analysis revealed that t he liver mitochondria and sinusoidal endothelial lining were better preserv ed after oxygen persufflation, which was in line with the data on enzyme re lease and the increased portal perfusion pressure in the untreated group, w hile normal values were found after venous systemic oxygen sufflation, Conclusion: Venous oxygen persufflation may thus represent a useful tool fo r the safe and improved preservation of ischemia-sensitive steatotic livers .