Kupffer cell function is important to overcome septic complications after partial liver resection

Abstract Background Intra-operative bile leakage testing is very important in partial liver resection in living donor liver transplant as it allows detection of bile leaking points on the cut surface and decreases postoperative bile leak which is one of the most dreadful complication following liver transplant surgery. In this study we tried to assess the Effectiveness of White test versus conventional saline test in minimizing biliary leak in partial liver resection in living donor liver transplant. Objective In this study, we assess whether the White test is better than the conventional saline test for the intraoperative detection of biliary leakage in patients who will undergo partial liver resection as living donor liver transplant. Methodology In this study, we assess whether the White test is better than the conventional saline test for the intraoperative detection of bile leakage in patients who underwent partial liver resection as a living donor liver transplant. This study included 60 patients who received partial liver resection as a living donor liver transplant. The conventional saline test (injecting an isotonic sodium chloride solution through the cystic duct) was carried out in 30 patients and the White test (injecting a fat emulsion solution through the cystic duct) was carried out in 30 patients Results Incidence of postoperative bile leakage was compared between the conventional method and the White test. Bile leakage occurred in 8 patients (26.7%) in the conventional method group and in 2 patients (6.7%) in the White test group. In addition, the White test detected intraoperative a significantly higher number of bile leakage sites compared with the conventional method. The White test is better than the conventional test for the intraoperative detection of bile leakage. Conclusion Based on our study, we recommend that surgeons investigating bile leakage sites during liver resections should use the White test instead of the conventional saline test.

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Mechanism of Hepatic Heme Oxygenase-1 Induction by Isoflurane

Anesthesiology ◽

10.1097/00000542-200601000-00016 ◽

2006 ◽

Vol 104 (1) ◽

pp. 101-109 ◽

Cited By ~ 24

Author(s):

Alexander Hoetzel ◽

Daniel Leitz ◽

Rene Schmidt ◽

Eva Tritschler ◽

Inge Bauer ◽

...

Keyword(s):

Nitric Oxide ◽

Protein Kinase C ◽

Protein Kinase ◽

Phospholipase A2 ◽

Heme Oxygenase ◽

Kupffer Cell ◽

Cell Function ◽

Heme Oxygenase 1 ◽

Gadolinium Chloride ◽

Kinase C

Background The heme oxygenase pathway represents a major cell and organ protective system in the liver. The authors recently showed that isoflurane and sevoflurane up-regulate the inducible isoform heme oxygenase 1 (HO-1). Because the activating cascade remained unclear, it was the aim of this study to identify the underlying mechanism of this effect. Methods Rats were anesthetized with pentobarbital intravenously or with isoflurane per inhalation (2.3 vol%). Kupffer cell function was inhibited by dexamethasone or gadolinium chloride. Nitric oxide synthases were inhibited by either N(omega)-nitro-L-arginine methyl ester or S-methyl thiourea. N-acetyl-cysteine served as an antioxidant, and diethyldithiocarbamate served as an inhibitor of cytochrome P450 2E1. Protein kinase C and phospholipase A2 were inhibited by chelerythrine or quinacrine, respectively. HO-1 was analyzed in liver tissue by Northern blot, Western blot, immunostaining, and enzymatic activity assay. Results In contrast to pentobarbital, isoflurane induced HO-1 after 4-6 h in hepatocytes in the pericentral region of the liver. The induction was prevented in the presence of dexamethasone (P < 0.05) and gadolinium chloride (P < 0.05). Inhibition of nitric oxide synthases or reactive oxygen intermediates did not affect isoflurane-mediated HO-1 up-regulation. In contrast, chelerythrine (P < 0.05) and quinacrine (P < 0.05) resulted in a blockade of HO-1 induction. Conclusion The up-regulation of HO-1 by isoflurane in the liver is restricted to parenchymal cells and depends on Kupffer cell function. The induction is independent of nitric oxide or reactive oxygen species but does involve protein kinase C and phospholipase A2.

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