BACKGROUND: in a hepa ic ischer fi>mperfusion (I/R) i~jury, massive Joss of thrombomo~ dulin (TM) t o m the sinusoida/endothelia] ceils aright be playing a central role in developing a liver damage especially ~l a warm ischemia of the graft trom non-Jmambeating donor Genet c modibcatior: o the liver graft to express exogenous TM might thus conmbure to an improvement of hepatic I/R ir~jury METttODS: Three groups ot 9 rats each underwent intra-venous in~ec ion of marke~ LacZ adeuovirus vector in Groupl (AxCAlacZ lX 109 cfuJ m[), human IM adenovims vector m Group 2 (AxCAhTM, I X 10 cfu/nt|), or normal saline in Grocp 3 (1 ml) For y-eigbt hrs atier gone transler, rats were anesthetized by ether and subjected to hepat c wa~-n ischerma of 30 rain. In all the groups, each 3 rats were sacrihced at 12 hrs, 24 his, and 7 days alter reperhision, to obtain the serum and hepatic tissue samples Serum samples were used to determine hepatic enzyme kvels, hyal'aroinc acid levels anti o t h e s Serum and hepatic tissue levels oi h-TM were also determined by an EL1SA (enzyme linked iramuno-.sorbent assay), Hepatic expression of Marker LacZ and hTM were also evaluated by a X-gal staining and immunnhistochemical staimng. RESULTS: Expression of marker LacZ (X-gai staining) in Group 1 and h-TM (immunohistochemical staining and R]'-PCR) m Group 2 were detected in the hver, until 7 days after hepatic ischemia Hepatic tissce blood flow (Laser Doppler) showed no difl}ren~e between the groups immediately niter reperfusion Serum ALT levels (205-+ 55 ILIA), hyaluronic acid (0 1 ] 8 2 007 ~gnll), and hepatic tissue blood flow were sigmficantly improved onIy in the hTM transiected Group 2, at 12 hrs alter repe~usion, CONCLUSION: These findings thus s~.ggested that adeuovi:rus mediated gone transfer oi h-TM helped to attenuate a liver damage, n the r a model ot warn ischemic liver injury,