Reliable Indices for the Determination of Viability of Grafted Liver Immediately After Orthotopic Transplantation Bile Flow Rate and Cellular Adenosine Triphosphate Level

Sumimoto, Kazuo; Inagaki, Katsuya; Yamada, Kazuo; Kawasaki, Takashi; Dohi, Kiyohiko

doi:10.1097/00007890-198810000-00007

Cited by 129 publications

(61 citation statements)

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“…65,66 The use of isolated perfusion to predict survival of steatotic livers before transplantation would merely require establishing parameters that correlate with survival. These may include hemodynamic parameters, 67 as well as markers of synthetic function 68 and liver injury 69 assessed by sampling perfusate. If a supply of oxygen and nutrients is provided within a suitable perfusate, then continual normothermic preservation may become a viable reality, thus abrogating the increased sensitivity of fatty livers to cold preservationreperfusion injury.…”

Section: Potential For Novel Preservation Methods and Amelioration Ofmentioning

confidence: 99%

Hepatic steatosis and its relationship to transplantation

Imber

Peter

Handa

et al. 2002

Liver Transplantation

150

108

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Section: Potential For Novel Preservation Methods and Amelioration Ofmentioning

confidence: 99%

Hepatic steatosis and its relationship to transplantation

Imber

Peter

Handa

et al. 2002

Liver Transplantation

150

108

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“…[1][2][3][4][5][6] Bile formation is an osmotic filtration-driven process that depends on the proper function of transport systems in both the basolateral and apical or canalicular membranes of hepatocytes. 7,8 Available experimental data show that bile secretory function is impaired after either warm or cold ischemia in rats.…”

mentioning

confidence: 99%

Bile secretory function after warm hepatic ischemia-reperfusion injury in the rat

Accatino¹,

Pizarro²,

Solı́s³

et al. 2003

Liver Transplantation

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Hepatic ischemia-reperfusion (I-R) injury frequently is associated with cholestasis. However, the underlying mechanisms are not fully understood. The aim of the study is to assess bile secretory function in vivo in rats subjected to warm lobar hepatic ischemia at different times during reperfusion. A model of lobar 70% warm hepatic ischemia for 30 minutes was used with studies conducted at 1 and 6 hours and 1, 3, and 7 days after reperfusion. Bile secretory function was assessed after selective cannulation of bile ducts of ischemic (ILs) and nonischemic lobes (NILs). Serum activity of hepatic alanine and aspartate aminotransferase was slightly increased in rats subjected to I-R, whereas serum bile salt levels increased early during reperfusion, returning to control values after 7 days. ILs showed mild reversible leukocyte infiltration and no significant necrosis. Bile flow and bile salt excretion were significantly decreased in ILs during the first 24-hour reperfusion period compared with shamoperated rats and NILs. A marked reduction in glutathione (GSH) excretion occurred at 1 and 6 hours and 1 and 3 days, which returned to control values after 7 days. Total GSH and both reduced and oxidized GSH levels in liver homogenate and arterial blood GSH levels were unchanged at all times. Protein mass of multidrug resistance protein 2 and its function, assessed by the hepatic maximum secretory rate of ceftriaxone, did not show significant changes in ILs or NILs compared with shamoperated rats. Liver tissue ␥-glutamyl transpeptidase (GGT) and ␥-glutamylcysteine synthetase activities remained unchanged, whereas biliary GGT and cysteine secretory rates were significantly increased in ILs and NILs. Administration of acivicin, a GGT inhibitor, resulted in decreased secretion of this enzyme into bile and a parallel marked increase in biliary GSH secretion compared with untreated ischemic rats. In conclusion, warm hepatic I-R induces reversible cholestatic changes in ILs. GSH secretory rates from both ILs and NILs were markedly decreased during reperfusion. The reversibility of this effect after GGT inhibition, as well as increased release of active GGT into bile and cysteine biliary secretory rates, suggest increased GSH degradation in bile. These findings might be relevant for the I-R-induced clinical cholestasis, as well as cholangiocyte injury, seen after hepatic ischemia. (Liver Transpl 2003;9:1199-1210.)

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“…Additional factors which may have facilitated bile production over the 3 h perfusion interval may include tissue oxygenation and its metabolic sequelae as well as actions of SAM aecting bile formation. Thus, oxygen extraction ratio values were higher for the (S,S) isomer than its (R,S) racemer over the 3 h perfusion period as a result of lower oxygen consumption and increased oxygen delivery and this may contribute to its greater choleretic activity via enhanced ATP production (Sumimoto et al, 1988). An additional consideration may be the participation of administered (S,S) SAM in transmethylation and trans-sulphuration reactions excluded to its (R,S) racemer by steric considerations (De La Haba et al, 1959;Homan, 1986) and of known bene®t to bile production (Friedel et al, 1989).…”

Section: Discussionmentioning

confidence: 98%

Evidence that S‐adenosyl‐L‐methionine diastereoisomers may reduce ischaemia‐reperfusion injury by interacting with purinoceptors in isolated rat liver

Dunne¹,

Berndt²,

Williams³

et al. 1998

British J Pharmacology

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Mechanisms underlying the haemodynamic activity of diastereoisomers of S‐adenosyl‐L‐methionine (SAM) were investigated using inhibitors of purinoceptors and nitric oxide (NO) synthase in perfused rat livers damaged by sequential 24 h cold and 20 min rewarming ischaemia+reperfusion. Stored livers were flushed with 10 ml saline alone (control) or with added (R,S) or (S,S) SAM (100 μM) and reperfused in the absence (control) or presence of 10 μM 8‐phenyltheophylline (8‐PT) or 100 μM L‐N‐monomethylarginine (L‐NMMA). Both SAM diastereoisomers rapidly increased blood flow and bile production versus controls (P<0.001) but the (R,S) isomer induced greater increases in blood flow and the (S,S) isomer greater increases in bile production: 625 versus 596 versus 518 ml blood flow and 100 versus 119 versus 56 mg bile production per g liver over 3 h in (R,S), (S,S) and control, respectively. 8‐PT prevented the enhancement of blood flow by (S,S) SAM (529 versus 596 ml g −1liver over 3 h for (S,S) SAM alone, P<0.001), but was without effect in control livers. 8‐PT also reduced SAM‐enhanced bile production: 51 versus 119 mg g −1liver over 3 h, P<0.001. L‐NMMA reduced blood flow and bile production similarly in the absence or presence of (S,S) SAM. Thus, SAM may improve liver perfusion after ischaemia‐reperfusion injury via stimulation of P1 (A2) purinoceptors at which SAM shows activity. The choleretic activity of (S,S) SAM is disproportionately greater than enhanced blood flow and may occur independently of a NO‐dependent component of bile production. British Journal of Pharmacology (1998) 125, 225–233; doi:10.1038/sj.bjp.0702043

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Reliable Indices for the Determination of Viability of Grafted Liver Immediately After Orthotopic Transplantation Bile Flow Rate and Cellular Adenosine Triphosphate Level

Cited by 129 publications

References 0 publications

Hepatic steatosis and its relationship to transplantation

Hepatic steatosis and its relationship to transplantation

Bile secretory function after warm hepatic ischemia-reperfusion injury in the rat

Evidence that S‐adenosyl‐L‐methionine diastereoisomers may reduce ischaemia‐reperfusion injury by interacting with purinoceptors in isolated rat liver

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