PP 64. Vascularisation Process after RMHV Ligation

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J. Arlt, H. Huang, D. Meihong, M. Thomas, R. Feuer, U. Dahmen, O. Dirsch

18:34 - 18:40h at Lanchid Room

Categories: Hepatobiliary and Pancreatic Surgery, Poster Session

Session: Poster (P5) - Hepatobiliary & Pancreatic Surgery

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Background
Previously we described the spontaneous vascularisation process following focal outflow obstruction induced by RHMV-ligation in rats (Dirsch (2008); Huang (2011)). Revascularisation was visualized using 3D-reconstructions of μ-CT scans obtained from corrosion casts. The aim of this work was to analyze the role of arterial perfusion for the spontaneous revascularisation process using the "Dynamic ArrayTM integrated fluidic circuits PCR"(Fluidigm).

Material and Methods
RMHV-ligation was performed in male Lewis rats. Additional partial hepatectomy and/or treatment with L-Name or molsidomine were performed in rats. Rats were sacrificed at 0h, 24h, 48h and 1week post-op (n=6). Samples were taken separately from the obstruction, border and normal zone. The mRNA expression of 96 genes, with special focus on markers of vascularisation (Laminin, vWF) and genes of differnt vascularisation processes was analyzed by Fluidigm. The LEM-method (Feuer (in process)) was used to normalize and to calculate the qPCR results.

Result
mRNA expression (35-fold increase) of the vascularisation markers Laminin was seen 24h after RMHV-ligation and PH and 48h after RMHV-ligation, PH and L-NAME treated rats in the obstructed zone. Substantially lower levels of vWF mRNA expression (max 7-fold at 48h) were seen in animals subjected to RMHV-ligation and liver resection only. Animals subjected only to RMHV showed a discrete and brief increase in gene expression.

Conclusion
Gene expression corresponded to the severity of hepatic arterial hypoperfusion caused by portal hypertension and L-NAME treatment. This finding suggests that laminin expression is related to relative hepatic hypoxia.