Effects of hemodynamic instability on brain death-induced prepreservation liver damage1

Golling, M.; Mehrabi, Arianeb; Blum, K.; Jahnke, Cosima; Kellner, H.; Bud, Octavian; Hashemi, Bahram; Breitkreutz, Raoul; Becker-Brandenburg, Katja; Schemmer, Peter; Gebhard, Martha Maria; Herfarth, Christian; Kraus, Thomas

doi:10.1097/01.tp.0000062868.34247.8f

Cited by 19 publications

(31 citation statements)

References 29 publications

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“…62,63 In such a scenario the effects of hepatic warm ischemia during IPC could be different from those in normotensive patients undergoing LR. Furthermore, brain death induces a multifaceted, intense systemic inflammatory response, which manifests in many organs, including the liver.…”

Section: Brain Death and Associated Pathophysiologymentioning

confidence: 99%

Ischemic preconditioning of the liver: A few perspectives from the bench to bedside translation

et al. 2008

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Utilization of ischemic preconditioning to ameliorate ischemia/reperfusion injury has been extensively studied in various organs and species for the past two decades. While hepatic ischemic preconditioning in animals has been largely beneficial, translational efforts in the two clinical contexts-liver resection and decreased donor liver transplantation-have yielded mixed results. This review is intended to critically examine the translational data and identify some potential reasons for the disparate clinical results, and highlight some issues for further studies.

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Section: Brain Death and Associated Pathophysiologymentioning

confidence: 99%

Ischemic preconditioning of the liver: A few perspectives from the bench to bedside translation

et al. 2008

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“…Following laparotomy and abdominal preparation, the abdomen was temporarily closed and the animal turned around. For brain death induction, we used a modified method as published recently 11. Briefly, 3 burr holes were placed (ø 1 cm) in the left temporal epidural with a Codman probe (Codman & Shurtleff, UK) and in the right temporal epidural with a 10‐French Foley catheter, as well as a left frontal intraparenchymal thermal diffusion probe (Thermal Technologies, Cambridge, MA).…”

Section: Methodsmentioning

confidence: 99%

“…Real‐time microperfusion was assessed (1/second) via a thermal diffusion probe (Thermal Technologies, Cambridge, MA) placed intrahepatically (20 mm) into the right median lobe of the liver. The method has been described before and is used routinely in our institution in all large animal experiments and clinical liver transplantation 11, 12, 17. The method for analyzing cerebral blood flow was essentially the same.…”

Section: Methodsmentioning

confidence: 99%

“…Under the title of prepreservation damage,6 both are closely linked to liver innervation 7–9. Brain death is commonly accompanied by hemodynamic instability10–12 and changes in splanchnic and pulmonary resistance, as well as neuroendocrine alterations 13, 14. When there is no systemic malperfusion due to hypotension, liver damage is mainly caused by a central impairment due to metabolic derangements and microcirculatory disturbances via efferent sympathetic nerves 2, 7, 9, 15.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2007

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The liver function and perfusion following brain death is mainly influenced by the sympathetic nerves and hormones. We examined the specific influence of surgical liver denervation on systemic and hepatic perfusion parameters, bowel ischemia and oxidative stress in hemodynamically stable BD and control (living donor [LD]) pigs. Brain death was induced in 8 pigs via saline infusion into the balloon of an epidural Tieman-catheter (1 mL/15 minutes) and compared to the control group (n ϭ 6) over 4 hours. At 2 hours postoperatively, complete liver denervation was initiated. We analyzed systemic cardiocirculatory parameters (mean arterial pressure, aortic flow, bowel ischemia (endotoxin, and endotoxin-neutralizing capacity) and oxidative stress (total glutathione in erythrocytes [tGSH E ]) and compared them to local/hepatic perfusion parameters (hepatic artery and portal venous flow, liver blood flow index, and microperfusion), local bowel ischemia (intramucosal pH [pHi] of stomach [pHi S ]/colon[pHi C ]), and liver oxidative stress (glutathione [rGSH L , GSSG L ]). Following brain death, the parameters including mean arterial pressure, aortic flow, pHi, endotoxin, and tGSH E showed no significant changes at 2 hours. Portal venous flow and microperfusion were decreased significantly and hepatic arterial buffer response was ineffective. Hepatic oxidative stress was increased in BD animals (2rGSH L , 1GSSG L ). Surgical denervation/manipulation increased portal venous flow significantly, hepatic arterial buffer response became effective, and stomach pHi decreased (BD and LD groups). Hepatic oxidative stress was reduced in the BD group (1rGSH L /GSSG L ; P Ͻ 0.001) while it was increased in the LD group (2rGSH L /GSSG L ; P Ͻ 0.001). In conclusion, denervation reduces hepatic oxidative stress in BD only in contrast to the LD. The reciprocal effect of denervation depends on the state of neural activation and postulates a potential benefit of surgical denervation before organ harvesting in brain death. Liver Transpl 13:607-617, 2007.

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“…The study by Compagnon et al [35], published in 2002, observed that there are no significant changes in AST, ALT, LDH, gamma-glutamyl transpeptidase (GGT), and total bilirubin (except for alkaline phosphatase (AKP)) before organ removal in brain-dead donors compared with those that have been brain dead for 16 h. After orthotopic transplantation of donor livers cold-preserved for 24 h in the University of Wisconsin solution, there were no significant differences in AST, ALT, and LDH in two groups, which gradually became normal after 2-3 days. Golling et al [36] reported in 2003 that aspartate aminotransferase/glutamate-oxaloacetate transaminase (AST/GOT) of hypotensive and normotensive brain-dead pigs both increased after induction of brain death. Olinga et al [18] showed there were no differences in the levels of ATP between brain-dead rat livers and liver from live rats; furthermore, brain death within 6 h does not influence the viability of the donor liver.…”

Section: Changes In Liver Functionsmentioning

confidence: 98%

The influence of brain death on donor liver and the potential mechanisms of protective intervention

Zhang

Wang

2011

Front. Med.

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Brain-dead donors have become one of the main sources of organs for transplantation in Western countries. The quality of donor organs is closely related to the outcome of the transplantation. Experimental studies have confirmed the inferior graft survival of livers from brain-dead donors compared with those from living donors. Studies conducted in the past 10 years have shown that brain death is associated with effects on the decreased donor organ quality. However, whether the decrease in the viability of donor organs is caused by brain death or by the events before and after brain death remains uncertain. The purpose of this review is to introduce the advances and controversies regarding the influence of brain death on the viability of donor livers and to summarize the mechanisms of the different protective interventions for donor livers.

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Effects of hemodynamic instability on brain death-induced prepreservation liver damage1

Cited by 19 publications

References 29 publications

Ischemic preconditioning of the liver: A few perspectives from the bench to bedside translation

Ischemic preconditioning of the liver: A few perspectives from the bench to bedside translation

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

The influence of brain death on donor liver and the potential mechanisms of protective intervention

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