| Literature DB >> 2256166 |
M Manner1, W Shult, N Senninger, G Machens, G Otto.
Abstract
The ischemic damage following liver transplantation (LTX) is predominantly located at the endothelial cell level and is a major cause for a disturbance of microcirculation. The present study was designed to test the hypothesis that changes in the quality of organ preservation are correlated with changes in microcirculation: 16 pigs underwent LTX, preservation by Bretschneider's HTK-solution (Histidin, Tryptophan, alpha-Ketoglutarat) complemented by indomethacin (50 mumol/L). Cold ischemia times were 9 hr (n = 8) and 18 hr (n = 8), respectively. Using the H2-clearance technique, hepatic microcirculation was measured before, 30 min, and 20 hr after LTX. Normal tissue perfusion was 107 +/- 16 ml/100 g/min, at 30 min posttransplantation 91 +/- 13 ml/100 g/min in the short-term and 48 +/- 7 ml/100 g/min in the long-term preservation group. Whereas no animal of the long-term preservation group survived longer than 8 hr, all animals of the short-term preservation group survived, and tissue perfusion could be measured 20 hr postoperatively (101 +/- 19 ml/100 g/min). At 30 min postoperatively, all surviving animals had tissue perfusion rates greater than 70, and all nonsurvivors had values below 60 ml/100 g/min. We conclude therefore that the extent of decrease of microcirculation after LTX may be a useful predictor of organ function and survival.Entities:
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Year: 1990 PMID: 2256166 DOI: 10.1097/00007890-199012000-00007
Source DB: PubMed Journal: Transplantation ISSN: 0041-1337 Impact factor: 4.939