No abstract

Donor hypernatremia was reported to cause postoperative graft dysfunction in human orthotopic liver transplantation (OLT). However, the effects of the correction of donor hypernatremia before organ procurement have not been confirmed. The aim of this study is to determine whether donor hypernatremia is associated with early graft dysfunction after OLT and to determine the effect of the correction of donor hypernatremia. One hundred eighty-one consecutive OLTs performed between May 1997 and July 1998 were entered onto this study. The cases were divided into three groups according to the donor serum sodium concentration: group A, serum sodium of 155 mEq/L or less before organ procurement (n ‫؍‬ 118); group B, peak sodium greater than 155 mEq/L and final sodium 155 mEq/L or less (n ‫؍‬ 36); and group C, final sodium greater than 155 mEq/L (n ‫؍‬ 27). Graft survival within 90 days after OLT and early postoperative graft function were analyzed. There were no significant differences in donor and recipient variables among the three groups. The frequencies of graft loss were 15 of 118 grafts (12.7%) in group A, 4 of 36 grafts (11.1%) in group B, and 9 of 27 grafts (33.3%; P F .05 v groups A and B) in group C. The liver enzyme values in groups B and C were significantly greater than those in group A postoperatively. The prothrombin times of group C were significantly longer than those of group A for the first 4 postoperative days. Recipients of hepatic allografts from donors with uncorrected hypernatremia had a significantly greater incidence of graft loss compared with recipients of hepatic allografts from normonatremic donors. However, the differences in graft survival were abrogated by the correction of donor hypernatremia before procurement. Copyright 1999 by the American Association for the Study of Liver DiseasesS everal retrospective analyses of donor and recipient variables have attempted to identify risk factors predictive of both patient and graft survival after orthotopic liver transplantation (OLT). To date, the following donor-associated risk factors have been shown to adversely affect patient or graft survival: donor age, 1,2 sex, 3,4 liver function test results, 5 cytotoxic cross-match, 6 length of intensive care unit (ICU) stay, 1 use of vasopressors, 7 and preservation time. 2,8,9 Previously, all these risk factors were considered static and not subject to manipulation by the procurement team, primarily because of time constraints. However, recent legislation requiring earlier notification of potential organ donors and earlier turnaround time for serum chemistries have provided additional time to manage brain-dead donors before organ procurement and correct such abnormalities as hypernatremia that may adversely impact on both graft and recipient survival.Uncorrected hypernatremia in organ donors has been associated with poor graft or patient survival in at least four studies. 7,9-11 These retrospective analyses suggested donor hypernatremia resulted in a greater incidence of early postoperative graft dys...

FME is useful for reducing intraoperative bleeding.

Hepatic allografts from donors who have suffered a brief cardiopulmonary arrest may sustain ischemic damage before organ procurement. However, there is no reported correlation between donor cardiopulmonary arrest and hepatic allograft dysfunction. On the other hand, brief ischemia-reperfusion injury has been shown experimentally to result in protection in several organ models. Induction of ischemic tolerance has been called ischemic precondition- Several retrospective analyses of donor and recipient variables have attempted to identify risk factors predictive of hepatic allograft outcome after orthotopic liver transplantation (OLT). 1-3 The influence of brief donor cardiopulmonary arrest is unclear. Although the hepatic allograft is damaged during this brief ischemic phase, there have been no reports showing a correlation between donor episode of cardiopulmonary arrest and hepatic allograft dysfunction.On the other hand, cardiac protection has been shown after brief periods of ischemia during ischemic preconditioning. [4][5][6] The ischemic preconditioning has not been described in human liver transplantation, whereas some investigators have reported this effect in the liver in small animal experiments. [7][8][9][10] This phenomenon may occur in hepatic allografts from donors who suffered a brief cardiopulmonary arrest.In this study, we attempted to investigate the influence of brief donor cardiopulmonary arrest on hepatic allograft outcome in human liver transplantation by means of prospective collection of donor and recipient data.

Background: The suppressed production of nitric oxide (NO), associated with endothelial dysfunction, is thought to be a cause of ischemia and reperfusion injury of the liver. But findings of the salutary effects of NO enhancement on such injury have been conflicting. In this study, we tested our hypothesis that NO enhancement would attenuate ischemic liver injury. For this purpose, an NO precursor, L-arginine, and a novel NO donor, FK409, were applied to a 2-hour total hepatic vascular exclusion model in dogs.