Intramucosal pH and liver endotoxin clearance during experimental liver transplantation

Abstract

The study was designed to concentrations were significantly assess the gastrointestinal ischaemia lower in the pretreated group and the influence of the specific [39 f 23 pg/ml (Control): 14 f 7 Kupffer cell toxin gadolinium chlo-(GdCI,); P < 0.051 suggesting an imride (GdC1,) on the hepatic and ex-proved liver LPS clearance [86% 051. The anhepatic phase in-24 h before explantation, while con-duced splanchnic ischaemia which trols (n = 8) received normal saline. correlated with portal endotoxaGastric and sigrnoid intramucosal emia. Donor preconditioning with pH (pHi), LPS and endotoxin-neu-GdCI, leads to lower systemic LPS tralising capacity (ENC) levels were concentrations in the recipient and measured in the portal vein and su-increases ENC values in the early perior vena cava after laparatomy, at phase after OLT. An improved the end of the anhepatic phase and hepatocellular LPS extraction a n d 1 h after reperfusion. During the or an activation of the extrahepatic anhepatic phase, the sigmoid pHi reticulo-endothelial system as a redecreased significantly from sult of GdC1, treatment is discussed.7.32 * 0.02 to 7.29 i 0.03 (P < 0.001) and was associated with a substan-

Reduced glutathione in the liver as a potential viability marker in non-heart-beating donors

“…During the “zero flow situation” of ATx, the pHi and LPS cannot be measured in donors. The pHi cutoff indicating survival proposed in our brain‐dead model (pH 7.28) was not confirmed 47. As in previous experiments, during extended use of the passive porto‐jugular VVB, a flow decrease of 20%‐30% was found in the recipient 47.…”

“…The pHi cutoff indicating survival proposed in our brain‐dead model (pH 7.28) was not confirmed 47. As in previous experiments, during extended use of the passive porto‐jugular VVB, a flow decrease of 20%‐30% was found in the recipient 47. This could have contributed substantially to the decrease in pHi and increase in LPS, and eventually to the decrease in survival in the NHBD‐90 group.…”

“…Changes in pHi, LPS, and ENC are considered valuable local and systemic markers of bowel ischemia, especially in the experimental setting 36–48. Although portal flow is substantially decreased during clamping and VVB, comparable flow during cardiodepression and brain death have shown that macrocirculatory changes in the portal circulation do not necessarily correlate with MP in the bowel mucosa and LPS levels 49, 50.…”

Distinct effects of surgical denervation on hepatic perfusion, bowel ischemia, and oxidative stress in brain dead and living donor porcine models

“…Interpretation of low endotoxin neutralizing capacity, the primary serum antagonist of endotoxin, is somewhat difficult. Levels may be increased or decreased in liver dysfunction,52, 53 dependent on the induction of protein synthesis inside and outside the liver 54. From previous animal studies, we could show a possible link between hepatocellular damage and the portosystemic endotoxin neutralizing capacity gradient,11, 51 but since systemic endotoxin did not increase, the persistent decrease of endotoxin neutralizing capacity is most likely to be due to sufficient neutralization of endotoxin in the portal and systemic circulation.…”