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PubMed2003

The superior results of living-donor renal transplantation are not completely caused by selection or short cold ischemia time: a single-center, multivariate analysis.

BACKGROUND: The results of living-donor (LD) renal transplantations are better than those of postmortem-donor (PMD) transplantations. To investigate whether this can be explained by a more favorable patient selection procedure in the LD population, we performed a Cox proportional hazards analysis including variables with a known influence on graft survival. METHODS: All patients who underwent transplantations between January 1981 and July 2000 were included in the analysis (n=1,124, 2.6% missing values). There were 243 LD transplantations (including 30 unrelated) and 881 PMD transplantations. The other variables included were the following: donor and recipient age and gender, recipient original disease, race, current smoking habit, cardiovascular disease, body weight, peak and current panel reactive antibody, number of preceding transplants and type and duration of renal replacement therapy, and time since failure of native kidneys. In addition, the number of human leukocyte antigen identical combinations, first and second warm and cold ischemia periods, left or right kidney and fossa, donor kidney anatomy, donor serum creatinine and proteinuria, and transplantation year were included. RESULTS: In a multivariate model, donor origin (PMD vs. LD) significantly influenced the graft failure risk censored for death independently of any of the other risk factors (P=0.0303, relative risk=1.75). There was no time interaction. When the variable cold ischemia time was excluded in the same model, the significance of the influence of donor origin on the graft failure risk increased considerably, whereas the magnitude of the influence was comparable (P=0.0004, relative risk=1.92). The influence of all other variables on the graft failure risk was unaffected when the cold ischemia period was excluded. The exclusion of none of the other variables resulted in a comparable effect. Donor origin did not influence the death risk. CONCLUSION: The superior results of LD versus PMD transplantations can be partly explained by the dichotomy in the cold ischemia period in these populations (selection). However, after adjustment for cold ischemia periods, the influence of donor origin still remained significant, independent of any of the variables introduced. This superiority is possibly caused by factors inherent to the transplanted organ itself, for example, the absence of brain death and cardiovascular instability of the donor before nephrectomy.

Adult↗

PubMed2005

Expanded criteria donor kidney allocation: marked decrease in cold ischemia and delayed graft function at a single center.

Expanded criteria donor (ECD) kidney allocation aims to increase utilization and facilitate placement. We implemented an ECD program for pre-consented candidates and studied whether ECD allocation decreased cold ischemia time and delayed graft function (DGF). We compared donor, recipient and transplant data for ECD transplants performed during the first year of our program to those performed in the preceding 5 1/2 years. Logistic regression identified risk factors for DGF. Of 356 candidates, 107 (30%) consented, 32 (9%) completed evaluation and 20 (6%) underwent ECD transplantation during the program's first year. The recent and historical ECD cohorts had similar donor and recipient characteristics, except that recent ECD recipients were older. The rate of donor kidney biopsy dropped from 85% to 24% (p < 0.001). Cold ischemia time decreased from 16.4 to 7.4 h (p < 0.001), as did the incidence of DGF from 43% to 15% (p = 0.031). Three independent risk factors for DGF emerged: recipient height (OR 1.21/10 cm; p = 0.008), >4 HLA mismatches (OR 20.46; p = 0.0033) and cold ischemia time (OR 1.24/h; p = 0.0036). We conclude the ECD designation provides a description of kidney quality that may obviate biopsy. ECD allocation decreased cold ischemia time and DGF, which may improve graft survival.

Aged↗

PubMed1993

Hepatic utilization of exogenous nucleotide precursors for restoration of ATP after cold ischemia in rats.

The study objective was to assess hepatic utilization of exogenous adenosine or adenine to enhance ATP recovery in rat liver after cold ischemia. ATP was measured noninvasively by 31P nuclear magnetic resonance (NMR) in perfused livers before and after 18 h of cold ischemia. The hepatocellular concentration of ATP during the initial postischemic reperfusion without adenosine or adenine coinfusion was 60% of that in fresh liver. The ATP increased significantly (P < 0.001) to 139% and 82% of baseline in postischemic livers coinfused for 90 min with adenosine or adenine (final concentration, 1 mmol/L), respectively. Less than 0.5% of the excess adenosine was catabolized to uric acid. In conclusion, adenosine and, to a lesser extent, adenine are salvaged by liver after extended cold ischemia to enhance ATP restoration. Provision of these ATP precursors, as components of an enteral formulation may facilitate the repletion of liver ATP and foster early resumption of liver function after an ischemic insult.

Adenine↗

PubMed1992

Oxygen free radical scavengers and reperfusion injury in dog lung preserved in cold ischemia.

Oxygen-derived free radicals are now considered important contributors to tissue injury associated with ischemia and reperfusion. The purpose of this study was to determine the influence of oxygen free radical scavengers on reperfusion injury. The left lower lobes of 15 canine lungs were isolated, preserved, and then reperfused for 120 minutes. Three groups of lobes were studied: Group 1 (n = 5), without ischemia, group 2 (n = 5) four hours of cold ischemia in Euro-Collins solution, group 3 (n = 5) four hours cold ischemia+oxygen free radical scavenger glutathione (0.1 nmol/L) given at the moment of perfusion. Extravascular lung water (grams per gram of blood-free dry lobe weight) after reperfusion was 2.82 +/- 0.32, 5.06 +/- 0.45, 4.21 +/- 0.33 for groups 1 through 3 respectively (p less than 0.001 group 1 versus group 2, p less than 0.001 group 2 versus group 3). Lung tissue lipid peroxidation, measured as thiobarbituric acid reactive material was 125 +/- 11, 270 +/- 30, and 185 +/- 17 nmol/g dry lobe weight for groups 1, 2 and 3 respectively (p less than 0.05 group 2 versus 1 and group 3 versus group 2). The data suggest that oxygen free radical scavengers attenuate reperfusion injury.

Animals↗

PubMed2002

Combined effects of fasting and alanine on liver function recovery after cold ischemia.

The effect of donor nutritional status on hepatic function recovery after cold ischemia is still debated. We demonstrated previously that a 48-h fast diminished the survival rate of liver-transplanted rats and that the deleterious effect of fasting was prevented by infusion of alanine to the recipient at reperfusion. Whether the duration of fasting influenced the protective effect of alanine and whether this effect was metabolic were not known, and the elucidation of these questions is the aim of this study. The effect on hepatic function recovery of fasting periods of 24 h, 48 h and 72 h prior to cold ischemia were studied in a model of isolated, perfused rat liver. After a cold-ischemic time of 24 h in University of Wisconsin (UW) solution at 4 degrees C, livers were reperfused for 3 h. The combined effect of alanine (8 mM) infusion at liver reperfusion was evaluated for each prior fasting period. The addition of pyruvate (8 mM), a metabolic intermediary of alanine, was only tested in the 72-h fasting group. The evaluation criteria were: liver weight after reperfusion, release of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) in the perfusate, bile production, vascular resistance and liver histology after reperfusion. The enzyme release at reperfusion was significantly higher when livers were harvested from rats submitted to a 48-h fast (ALT) or a 72-h fast (ALT, AST, LDH), as compared to those from fed rats. Vascular resistance was increased in 72-h fasted livers. An addition of alanine (8 mM) at reperfusion lowered the release of AST, ALT and LDH. This effect was more obvious when the fasting duration was increased. By contrast, the addition of pyruvate at reperfusion did not improve the recovery of livers submitted to a 72-h fasting period before preservation. A long fasting period is deleterious as compared to feeding; however, this effect can be compensated by infusion of alanine at reperfusion. The mechanism involved is not metabolic. In a clinical setting, the infusion of alanine to the recipient at reperfusion may be a convenient way to compensate for donor undernutrition, especially after a long stay in an intensive care unit.

Alanine↗

PubMed1998

Effect of ischemic preconditioning on hepatic tolerance to cold ischemia in the rat.

A short warm ischemia before reperfusion has been shown to improve the tolerance of the heart and the liver to a prolonged warm ischaemia. The present experimental study was conducted to evaluate the effect of such preconditioning on hepatic tolerance to an extended cold ischemia. In a model of isolated perfused liver, livers from Wistar rats (250-350 g) were stored for 24 h in UW (4 degrees C) immediately after harvesting and reperfused for 3 h at 37 degrees C. Control livers subjected to a 24-h cold ischemia were compared to livers subjected to preconditioning (defined as a 5- or 10-min clamping of the hepatic pedicle followed by a 10-min reperfusion before liver harvesting) prior to the definitive 24-h cold ischemia. While there was no difference in bile production between the preconditioned groups and the controls, transaminases and LDH release was significantly increased, vascular resistance was enhanced, and preservation injury was more extensive in both preconditioned groups as compared to controls. In contrast to the beneficial effect reported on prolonged warm ischaemia, preconditioning has a deleterious effect on hepatic tolerance to an extended cold ischemia.

Animals↗

PubMed1999

Late graft dysfunction after prolonged cold ischemia of the donor kidney: inhibition by cyclosporine.

BACKGROUND: The present study was devised to elucidate the influence of prolonged cold ischemia on the development of chronic transplant dysfunction (CTD) in kidney isografts (Brown Norway-->Brown Norway; BN-->BN) and in kidney allografts (BN-->Wistar Agouti/ Rij [WAG]) under temporary cyclosporine (CsA) therapy. METHODS: To induce ischemic injury, BN donor kidneys were preserved for 24 hr in 4 degrees C University of Wisconsin solution before transplantation. Renal function (proteinuria), histomorphology according to the BANFF criteria for CTD, and infiltrating cells were assessed. Grafts were examined both early at days 2, 3, 6, and 10, and late at week 26 (allografts) or at week 52 (isografts). RESULTS: Nonischemic isografts preserved a normal function and morphology. Ischemic isografts developed a progressive proteinuria over time and demonstrated significantly more glomerulopathy with macrophage (Me) infiltration and intimal hyperplasia than nonischemic controls at week 52. During the initial 10 days, there was an increased infiltration of MHC class II+ cells, predominantly CD4+ cells and Mphi, coinciding with up-regulated intercellular adhesion molecule-1 expression. CsA treatment in ischemic isografts inhibited infiltration of MHC II+ cells in the early stage, which was accompanied by significantly less renal damage at week 52 compared with untreated controls (proteinuria: 59+/-8 vs. 134+/-19 mg/24 hr; BANFF score: 2.8+/-0.4 vs. 4.3+/-1.0). Under CsA therapy, 24-hr cold ischemia of the allograft affected neither the onset or progress of proteinuria, nor the histomorphology (BANFF score: 7.8+/-2.4 vs. 7.3+/-1.9). In both ischemic and nonischemic allografts, intercellular adhesion molecule-1 expression and mononuclear cell infiltration (CD4, CD8, Mphi was abundantly present during the first 10 days and function deteriorated rapidly. CONCLUSIONS: Prolonged cold ischemia plays a role in the induction of CTD, but its deleterious effect can be successfully inhibited by CsA. Therefore, the alloantigeneic stimulus is the overriding component in the multifactorial pathogenesis of CTD.

Adenosine↗

PubMed1995

The effect of nicardipine on renal functions following 72-hour cold ischemia.

The aim of the study was to investigate the cytoprotective effect of a calcium channel blocker, nicardipine, on altered renal function due to cold ischemia for 72 h. The experiments were performed on isolated perfused kidneys from adult rabbits. Kidneys were perfused with either standard Euro-Collins (EC) solution (n = 7) or EC containing nicardipine (n = 6) and then incubated with the same preservation solutions in a beaker exposed to cold ischemia for 72 h at +4 degrees C. In the control group the same procedure was applied to untreated kidneys (n = 6) which were exposed to cold ischemia for 30 min. Vascular responses and urinary output to noradrenaline, angiotensin II, endothelin-1, acetylcholine and sympathetic stimulation were assessed as the functional activities of the kidney. The responses of the preserved kidneys were compared following cold ischemic conditions. The results indicate that the addition of nicardipine to EC solution protects the vascular endothelial regulatory function and urine excretion; therefore, dihydropyridine calcium channel blockers might be useful for kidney preservation.

Animals↗

PubMed2004

Application of sulforaphane--does it lead to improvement of islet graft survival after warm and/or cold ischemia.

OBJECTIVES: Brain stem death results in ischemic damage of organs. To prevent many agents are being tested this damage. The aim of our study was to determine effects of sulforaphane (SF) on recovery, viability, lipid peroxidation, metabolic and endocrine function of islets isolated from rat pancreata and treated with warm and/or cold ischemia and then transplanted syngeneically. METHODS: Rat pancreata were recovered from non-heart beating rats after intraducatal injection of collagenase solution after 15 or 30 minutes of warm ischemia time (WT). Cold ischemia (CT) was obtained by storage of distended and harvested glands in tubes with UW solution in 4 degrees C for 120 minutes. Sulforaphane was administered 24 hours before isolation islets in concentration 24mg/kg b.w. Diabetes was achieved by intravenouse injection of streptozotocin (STZ 65mg/kg b.w.). Islets were transplanted into the liver through the portal vein. Experimental protocol included four groups: Group I: fresh pancreata not treated with SF, WT=0, CT=0; Group II: 15 or 30 min. of WT, with or without SF; Group III: 15 or 30 min. of WT and 120 min. of CT, with or without SF; Group IV: 120 min. of CT, with or without SF RESULTS: Stimulation index in all groups with sulforaphane was larger from 1.0 (normal response of islets on high concentration glucose in medium). Metabolic activity (MTT) in group II (WT15, SF), gr. IV (CT, SF) and in gr. III (WT15, CT, SF; p>0.05) was lower compared to control group (I). The concentration of MDA in groups with SF increased as compared to controls. The highest recovery and cell viability was observed in group IV (CT, SF) and in gr. III (WT15, CT, SF; p<0.05). In groups exposed to 30 min. of warm ischemia and/or 120 min. of cold preservation was observed higher % of dead islets cells. In vivo study shows that islets graft isolated from rat pancreata treated with sulforaphane reverse diabetes. CONCLUSIONS: Based on results we can conclude that SF in concentration 24mg/kg b.w. reveals protective effect on preserved pancreas and may have a potential clinical implication to improve hemodynamically unstable pancreas donor condition.

Animals↗

PubMed1996

Kinetics of cellular viability in warm versus cold ischemia conditions of kidney preservation. A biometric study.

We have determined the kinetics of the cellular viability ratio (CVR), defined as the number of living cells over the total cell count, in pig kidneys using propidium iodide and fluorescein diacetate staining, as a function of time and preservation conditions. The kidneys were preserved in warm or cold ischemia in order to mimic the conditions of transplantation from non-heart-beating donors or multiple removal with optimal preservation of the graft, respectively. To determine the CVR, the cells were obtained by a fine-needle aspiration biopsy, which minimizes the damage to the graft. A biometric analysis by regression enabled the determination of the time dependence for warm ischemia (CVR(t) = 80.0 x e(-0.733-t)(+2.7/-0.36)) and for cold ischemia (CVR(t) = 80.0 x e(-0.022-t)(+1.57/-0.64)) with a confidence interval of 95%. These master curves allow us to predict, under the described conditions, the CVR after a given ischemia time. The half-life of the cells can be deduced from the time-dependent CVR(t), and is 0.64 hr (38 min) for warm ischemia and 21.4 hr for cold ischemia. Further, the CVR for a given kidney can be used to assess its condition at removal: if the CVR is below 48% at 2 hr after removal, one can conclude that the organ has suffered a period of warm ischemia.

Animals↗

PubMed2004

A simple scoring system to evaluate the effects of cold ischemia on marginal liver donors.

BACKGROUND: Exactly what constitutes a marginal donor remains ill defined. The authors set out to create a scoring system that objectively classifies a donor as marginal or nonmarginal and to define what the maximum acceptable preservation period is for the marginal liver to minimize early graft dysfunction. METHODS: The authors performed an analysis on data collected prospectively of 397 cadaveric liver transplants. Both univariate and multivariate analyses were performed on donor, recipient, and perioperative factors with relation to early allograft dysfunction. A score was developed that classified donors into marginal and nonmarginal populations, and the influence of cold ischemia was determined for each group. RESULTS: Multivariate analysis-determined donor age and steatosis (moderate to severe) were independent predictors of deranged function. This enabled the authors to produce a scoring system to differentiate marginal donors with respect to risk of early allograft dysfunction as follows: Formula=(20.06xsteatosis)+(0.44xdonor age), cutoff 23.1. In the marginal group, the cutoff value of cold ischemia time was 12.6 hr. CONCLUSIONS: The authors developed a scoring system that classified an organ as marginal or nonmarginal depending on the donor age and degree of steatosis. Marginal livers have a strong risk of developing early allograft dysfunction with increasing cold ischemia times and should be transplanted within 12 hr. Cold ischemia time was not found to be an important factor in the development of early allograft dysfunction in nonmarginal donors.

Adolescent↗

PubMed2006

Inhibition of phospholipase C attenuates liver mitochondrial calcium overload following cold ischemia.

BACKGROUND: Graft failure due to cold ischemia (CI) injury remains a significant problem during liver transplantation. During CI, the consumption of ATP and the increase in cellular Ca concentration may result in mitochondrial Ca (mCa) overload through the mCa uniporter, which can ultimately lead to apoptosis and graft nonfunction. We recently identified phospholipase C-dl (PLC-dl) as a novel regulator of mCa uptake in the liver, and now extend those studies to examine the role of mitochondrial PLC in liver CI injury. METHODS: Rat livers were perfused with University of Wisconsin (UW) solution. Half was homogenized immediately; the other half was cold-stored for 24 hr in UW. Mitochondria were extracted by differential centrifugation and incubated in buffer containing ATP and 0.1 or 0.2 microM Ca. The selective PLC inhibitor, U-73122, was added to determine the effects of PLC inhibition on mCa uptake following CI. Western blots and densitometry quantified mitochondrial PLC expression. Mito Tracker Red fluorescence microscopy was used to verify mitochondrial transmembrane potential. RESULTS: Twenty-four hour CI caused a significant increase in mCa uptake (P<0.001), and increasing extramitochondrial Ca potentiated this effect. The PLC inhibitor, U-73122, decreased mCa uptake in nonischemic mitochondria (P<0.001), and had a greater effect on CI mitochondria (P<0.001). Mitochondrial PLC-dl expression increased 175+/-75% following CI (P<0.05). CONCLUSIONS: These data demonstrate that PLC-dl is essential for mCa uptake following CI, and that the PLC pathway may be sensitized by CI. The CI-induced increase in mitochondrial PLC-delta1 expression represents a novel mechanism whereby mCa uptake can increase independently of cytosolic conditions.

Adenosine Triphosphate↗

PubMed2005

Role of cold ischemia in acute rejection: characterization of a humoral-like acute rejection in experimental renal transplantation.

The aim of the study was to characterize the role of cold ischemia in the process of acute rejection using an experimental renal transplant model. Syngeneic renal transplants were performed between Wistar Agouti rats and allogeneic grafts using Wistar-Agouti rats as recipients of Brown-Norway kidneys. For cold ischemia (CI), kidneys were preserved in Euro-Collins (4 degrees C/ 2.5 hours). Rats were bilaterally nephrectomized at the moment of renal transplant and did not receive any immunosuppressant. The groups were NoAR (n = 6): immediate syngeneic transplant; CI-NoAR (n = 6): syngeneic transplant with CI; AR (n = 13): immediate allogeneic graft; CI-AR (n = 6): allogeneic graft with CI. Allogeneic rats were followed for the survival study. Syngeneic rats, with mean survival time beyond 6 months, were sacrificed on the day 7 to compare grafts with those in the allogeneic groups. H&E- and PAS-stained grafts were evaluated using the Banff criteria. Tissue INF-gamma and TNF-alpha were quantified by RT-real time-PCR on the kidney grafts. Renal insufficiency did not appear in the NoAR group, but it did from the posttransplant day 5 in both acute rejection groups. While NoAR kidneys showed well-conserved renal architecture, then AR group displayed variable degrees of tubular necrosis with scarce cellular infiltration, interstitial hemorrhage, vascular damage with fibrinoid necrosis, perivascular edema, and nuclear disruption. Cold ischemia in rejecting animals increased the mortality rate due to renal insufficiency and accelerated acute rejection. Independently of CI, the proinflammatory cytokines TNF-alpha and INF-gamma were increased in both rejection groups. In conclusion, addition of CI overactivates the acute rejection process via a humoral component.

Acute Disease↗

PubMed2003

Altered ATP-dependent mitochondrial Ca2+ uptake in cold ischemia is attenuated by ruthenium red.

BACKGROUND: Graft dysfunction as a result of preservation injury remains a major clinical problem in liver transplantation. This is related in part to accumulation of mitochondrial calcium (Ca(2+)), which has been linked to activation of proapoptotic factors. We hypothesized that cold ischemia increases mitochondrial Ca(2+) uptake in a concentration dependent fashion and that ruthenium red (RR) will attenuate these changes by inhibiting the mitochondrial Ca(2+) uniporter. METHODS: Rat livers perfused with cold University of Wisconsin (UW) solution (4 degrees C) with or without RR (10 microM) via the portal vein (n = 3 per group) were processed immediately (no ischemia) or after 24 h cold-storage (24 h cold ischemia). Mitochondria were separated by differential centrifugation, and adenosine triphosphate (ATP)-dependent (45)Ca(2+) uptake was determined in the presence of ATP (5 mM), adenosine diphosphate (ADP), or adenosine 5'-beta,gamma-imidotriphosphate (AMP-PNP); variable concentrations of extramitochondrial (45)Ca(2+) were used. All measurements were performed in triplicate. Student's t test with P < 0.05 was taken as significant. RESULTS: Our data demonstrate the following: 1) ATP-dependent (45)Ca(2+) uptake in mitochondria separated from livers following 24 h of cold ischemia in UW alone was higher than in mitochondria isolated from non-ischemic livers; the increased uptake was dependent on the concentration of (45)Ca(2+) in the incubation buffer. 2) There was no difference in ATP-dependent (45)Ca(2+) uptake between nonischemic mitochondria and those separated from livers stored in UW-RR for 24 h. 3) (45)Ca(2+) uptake in mitochondria from livers subjected to 24 h of cold ischemia in UW-RR was significantly lower compared to those from livers stored in UW alone when (45)Ca(2+) concentrations were greater than 1 microM. CONCLUSION: 1) Cold ischemia affects mitochondrial Ca(2+) handling, especially when it is challenged by high extramitochondrial Ca(2+) concentrations. 2) The addition of RR in preservation solution attenuates the effects of cold ischemia on mitochondrial Ca(2+) handling. 3) Inhibition of mitochondrial Ca(2+) uniporter with RR protects mitochondria from Ca(2+) overload at high Ca(2+) concentrations. These findings may offer a potentially effective strategy for prevention of ischemia-reperfusion injury in liver transplantation.

Adenosine Triphosphate↗

PubMed2002

Hyperthermia preconditioning induces renal heat shock protein expression, improves cold ischemia tolerance, kidney graft function and survival in rats.

BACKGROUND: Evidence indicates that hyperthermia preconditioning (HP) can be protective in kidney transplantation, possibly through increased heat shock protein (HSP) expression. A detailed study about individual HSPs and functional preservation is lacking, however. Therefore, we studied the effects of HP on kidney graft survival, function and HSP expression. METHODS: Male Lewis rats were or were not subjected to whole-body hyperthermia 24 h prior to kidney procurement. Kidneys were stored in UW solution at 4 degrees C for 32, 40 or 45 h. Recipient kidneys were both removed and single isografts transplanted orthotopically. RESULTS: HP strongly induced HSP72 and HSP32 expression. Following 32-hour cold ischemia, most animals survived even without prior HP. However, HP strongly reduced functional impairment induced by cold ischemia. Following 40-hour cold ischemia, kidneys from donors without HP did not recover function and all animals died within 3 days. In contrast, HP-exposed kidneys tolerated 40-hour storage significantly better, with 44% of rats surviving until sacrifice on day 7. In these animals, renal function was still better compared to animals with 32-hour-stored kidneys without HP. Histological alterations were also diminished following HP. CONCLUSION: Our data show that HP induces renal HSP72 and, for the first time, HSP32. HP increases survival following transplantation and acts by improving several parameters of kidney function including proteinuria, volume output and creatinine clearance.

Animals↗

PubMed1991

Effect of cold ischemia time on the early outcome of human hepatic allografts preserved with UW solution.

Five hundred ninety-three cadaveric livers were used for primary liver transplantation between October 24, 1987, and May 19, 1989. The grafts were procured with a combined method, using in situ cooling with cold electrolyte solution and backtable flushing with UW solution. The mean cold-ischemia time was 12.8 (range 2.4-34.7) hr. The cases were divided into 5 groups according to the cold-ischemia time: group 1: less than 10 hr (n = 223); group 2: 10-14 hr (n = 188); group 3: 15-19 hr (n = 101); group 4: 20-24 hr (n = 52); and group 5: greater than or equal to 25 hr (n = 29). There was no difference between the 5 groups in 1-year patient survival, highest SGOT in first week after operation, and SGOT and total bilirubin during the first month after operation. However, with a logistic regression model, the retransplantation rate (P = 0.001) and primary nonfunction rate (P = 0.006) significantly rose as cold-ischemia time increased, meaning that the equivalency of patient survival was increasingly dependent on aggressive retransplantation.

Adenosine↗

PubMed2002

Carolina rinse solution minimizes kidney injury and improves graft function and survival after prolonged cold ischemia.

BACKGROUND: Kidney damage caused by cold ischemia-reperfusion injury promotes adverse outcomes after renal transplantation. The purpose of this study was to determine whether Carolina rinse solution (CRS) used at the end of cold ischemic storage decreases kidney injury and improves graft function and survival. METHODS: Inbred male Lewis rats were used as donors and recipients. Left kidneys were removed from donor rats, infused with cold University of Wisconsin solution, and stored for 24, 30, or 48 hr at 0-1 degrees C. Just before implantation, kidneys were flushed with either Ringer's solution or CRS at 35-37 degrees C or were not treated. Kidneys were then transplanted into recipient rats with removal of both native kidneys. RESULTS: Survival and renal function were analyzed over a 14-day postoperative period. Among rats receiving kidneys after 24-hr cold storage, creatinine clearance was 75% greater in rats transplanted with kidneys flushed with CRS compared with Ringer's solution or nontreatment. In animals receiving kidneys after 30-hr cold storage, recipient survival after CRS was significantly higher than with Ringer's solution or without flushing (80% vs. 25% and 17%, respectively). However, CRS failed to prevent renal graft failure after 48 hr of cold storage (14% survival with CRS vs. 0% with Ringer's solution). In separate ex vivo studies, nonviable cell nuclei were labeled by trypan blue after cold preservation and brief warm reperfusion. CRS decreased podocyte and peritubular endothelial cell killing associated with cold ischemia-reperfusion injury. CONCLUSION: Flushing renal explants with warm CRS before implantation diminishes cold ischemia-reperfusion injury and improves the function and survival of transplanted kidneys.

Albuminuria↗

PubMed2003

Matrine protects sinusoidal endothelial cells from cold ischemia and reperfusion injury in rat orthotopic liver transplantation.

The effect of matrine on cold ischemia and reperfusion injury of sinusoidal endothelial cells (SEC) was investigated in rats using an orthotopic liver transplantation (OLT) model. Syngeneic Sprague-Dawley (SD) rats were randomly assigned to 4 groups of 32 rats: untreated group (controls), low-dose treated group, high-dose treated group, and sham operation group (normals). After 5 hr of preservation in Ringer's solution, orthotopic implantation of the donor liver was performed. At 1, 2, 4, and 24 hr after reperfusion, 6 rats from each group were killed to collect blood and to excise the median hepatic lobe; the other 8 rats were observed to assess the 1-wk survival rate post-transplantation. All transplant recipients in the untreated group (controls) died within 48 hr, mostly between 10 to 20 hr. Matrine treatment increased the 1-wk survival rate to 75% in both treated groups. Plasma levels of hyaluronic acid (HA) at 1, 2, and 4 hr post-implantation were decreased significantly by matrine treatment. The immunohistochemical expression of intercellular adhesion molecule-1 (ICAM-1) in rat liver decreased significantly in both treated groups, and the pathological changes of SEC were ameliorated. Matrine markedly inhibited the activation of Kupffer cells and their release of tumor necrosis factor (TNF). Hepatic malondialdehyde (MDA) levels and superoxide dismutase (SOD) activities were improved by matrine administration. In conclusion, matrine can protect SEC from cold ischemia and reperfusion injury after rat orthotopic liver transplantation.

Alkaloids↗