[The significance of the liver for the course of SIRS (Systemic Inflammatory Response Syndrome) following shock, trauma and during sepsis].
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Bacterial Infections↗
Biomedical subjects
I Marzi
Publications and source records attributed to I Marzi.
[The leukocyte-endothelial interaction as an expression of a hepatic inflammation reaction during an experimental shock syndrome].
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Endothelium, Vascular↗
Dose-related pattern of sinusoidal leukocyte adhesion in sublobular regions of the liver after systemic endotoxin challenge in the rat.
The unique arrangement of large numbers of fixed tissue macrophages, endothelial, and parenchymal cells along hepatic sinusoids as well as their key role in the acute phase response makes the liver a primary target organ in endotoxemia. Pathogenesis of hepatic failure in endotoxemia is incompletely understood, but microcirculatory failure as well as leukocyte-endothelial interaction in response to inflammatory mediators may relate to it. Using intravital fluorescence microscopy, sinusoidal widths, leukocyte flow velocity, and sublobular leukocyte (white blood cell (WBC)) adhesion characteristics 1 h after randomized intravenous application of 0, 0.1, 1, or 5 mg/kg b.w. Escherichia coli endotoxin O 111 B4 (ETX) were evaluated in female Sprague-Dawley rats (n = 6-8/group). Whereas the bolus injection of ETX caused only minor concurrent macrohemodynamic effects, a significant increase of permanent WBC adhesion especially in periportal areas (0 mg, 2.1 +/- 0.7%; 0.1 mg, 16.2 +/- 3.6%**; 1 mg, 15.5 +/- 1.0%**; 5 mg, 13.2 +/- 2.3%* (**p < .01, *p < .05, compared to vehicle)) was found in all groups 60 min after ETX challenge. In contrast, an increase of WBC margination in midzonal and pericentral regions was only seen with the higher doses of 1 or 5 mg/kg ETX, respectively. The sublobular pattern of WBC margination is consistent with the concept of regulation of WBC adhesion by inflammatory mediators released by lipopolysaccharide-stimulated Kupffer cells in vivo. We propose that overwhelming the detoxifying capacity of predominantly periportally located Kupffer cells with large amounts of ETX may lead to activation of pericentral-located resting macrophages paralleled by a rise of adhering leukocytes.
Animals↗
Endothelin-1 is involved in hepatic sinusoidal vasoconstriction after ischemia and reperfusion.
Endothelin-1 (ET-1), a vasoactive peptide, causes a significant rise in portal vein pressure, which is most likely a result of severe vasoconstriction in the liver. In this study, the effect of ET-1 on sinusoidal vasoconstriction in the liver after ischemia and reperfusion was directly investigated using intravital microscopy. In anesthetized female Sprague Dawley rats (200-250 g) ischemia of the median and left liver lobes was induced for 90 min by temporary ligation of the left pedicle. After declamping and a 90-min reperfusion period, the livers were exposed for intravital microscopy. Using a Nikon MM-11 fluorescence microscope (545 nm, 330x), a CCD camera (Cohu FK 6990), and a SVHS video recording unit, the hepatic microcirculation was directly investigated. Besides sham groups, two ischemia groups were studied, receiving ET-1 antiserum (anti-ET-1; 0.5 ml; Peptide Inst., Osaka, Japan) or NaCl 0.9% (0.5 ml) 5 min prior to reperfusion of the liver (n = 6/group). Following a transient drop in the mean arterial blood pressure in the anti-ET-1-treated groups, comparable systemic hemodynamic conditions among the four groups were noted during intravital microscopic assessment at the end of the 90-min reperfusion period. Reduction in the sinusoidal diameters during postischemic reperfusion (7.7 +/- 0.5 microm) was prevented by anti-ET-1 treatment (9.6 +/- 0.25 microm; P < 0.01; mean + SEM) back to control values (9.6 +/- 0.32 microm), while most of other microcirculatory parameters did not show significant differences. The results supported further the role of ET-1 in dysregulation of the sinusoidal vascular tone in the liver, e.g., after ischemia and reperfusion.
Animals↗
[Involvement of platelet activating factors in pathologic leukocyte-endothelium interactions in the liver after hemorrhagic shock].
INTRODUCTION: Microcirculatory disturbances and increased adhesion of leukocytes to the hepatic endothelium immediately following hemorrhagic shock have been observed. It is currently discussed, that mediators released by activated macrophages may have regulative functions for these alterations. The aim of the study performed was to investigate the effects of platelet activating factor (PAF) by application of PAF-receptor antagonists in respect to disorders of liver microcirculation and leukocyte adhesion following hemorrhagic shock. METHODS: Sprague-Dawley rats, anesthetized with pentobarbital, were exposed to hemorrhagic shock by depression of the mean arterial blood pressure (MABP) to 40 mmHg for 60 min by controlled blood removal. Three hours following adequate volume replacement together with blood retransfusion (60%) and at normalized MABP as well as supranormal cardiac output levels, the livers of the animals were investigated by intravital microscopy in respect to leukocyte adhesion and microcirculation. Evaluation of the microcirculation of 5 liver lobules/animal was performed on SVHS recorded images using a computer-assisted image analysis system. Three shock groups (n = 6 rats) and one sham-operated control group (n = 8) were compared. Shock/NaCl group received 0.1 ml NaCl 0.9% 15 min prior to shock induction and 1 min prior to shock therapy i. v., respectively. Shock/BN group received a total of 10 mg/kg of the PAF-antagonist BN 52021 (Dr. Braquet, Paris) and Shock/WEB group 2 mg/kg of the PAF antagonist WEB 2086 (Boehringer, Ingelheim), respectively in 2 injections with identical volume. RESULTS: The course of hemodynamic parameters MABP and cardiac output were comparable in all 3 shock groups. Metabolic parameters such as acid-base state and hematocrit values did not reveal differences. Evaluation of liver microcirculation indicated in all shock groups a reduction of sinusoidal diameters and a slight increase of velocity of leukocytes. The significantly increased temporary adhesion of leukocytes with an adhesion time shorter than 20s in the shock/NaCl group (adhesion index 154.1 +/- 63.2s/100 leukocytes; mean +/- SD) was reduced significantly by the PAF antagonists BN 52021 (82.2 +/- 24.2) and WEB 2086 (86.0 +/- 30.0). Permanent adhesion with an adhesion time longer than 20s was increased significantly particularly in zone I of the liver acinus (portal region) in all shock groups without specific effects of the PAF antagonists. CONCLUSIONS: Liver microcirculation following adequately treated hemorrhagic shock was disturbed, as indicated by narrowed sinusoids and increased adhesion of leukocytes. PAF seems to have no effect on sinusoidal narrowing in this period, however, it seems involved in temporary adhesion of leukocytes. The relevance of these early changes following hemorrhagic shock in respect to the development of organ dysfunction should be further addressed.
Animals↗
Involvement of oxygen radicals in shock related cell injury.
Shock-related organ failure evolves from a variety of starting points--ischemia, reperfusion, non-bacterial or bacterial inflammation--several mechanisms are involved. In addition to the effects of xanthine oxidase after ischemia/reperfusion, toxic oxygen species from phagocytes that accumulate in both intra- and extravascular tissue spaces are of central importance. A critical event is the contact (adhesion) of leukocytes to endothelial cells, which consequently are the targets for leukocyte products. Damage of membranes by lipid peroxidation and by exposure to mediators such as platelet activating factor (PAF), leukotrienes and proteases, leads to increased permeability, tissue oedema and organ dysfunction. Thus antioxidants and other agents that control phagocyte function are likely to contribute to the protection of the permeability barrier in shock states.
Burns↗
Value of superoxide dismutase for prevention of multiple organ failure after multiple trauma.
In a prospective, randomized trial, recombinant human superoxide dismutase (rhSOD, 3000 mg/day, Grünenthal, Aachen, Germany) or placebo was given intravenously during 5 days after multiple injuries (Injury Severity Score [ISS] > or = 27; 24 patients). Manifestation of multiple organ failure (MOF) and posttraumatic inflammatory response were evaluated over 14 days. No side effects were noted by continuous infusion of rhSOD, which allowed high SOD plasma levels (24.77 +/- 9.43 mg/L) compared with controls (0.03 +/- 0.02 mg/L). Multiple organ failure was attenuated by rhSOD treatment in respect to cardiovascular and pulmonary functions. Additionally, intensive care therapy was shortened from 30 days (Q25: 15; Q75: 37) to 21 days (Q25: 12; Q75: 41). A secondary increase of inflammatory mediators (e.g., C-reactive protein, polymorphonuclear [PMN]-elastase, phospholipase A2), as observed at the end of the first week in the placebo group, was reduced by rhSOD therapy. The results reveal an attenuation of organ failure after trauma, most likely by decreasing the release of inflammatory mediators and reduction of leukocyte-mediated organ injury. These preliminary results, while promising, need to be confirmed in a larger number of patients.
Acute-Phase Reaction↗
Macrophage activation and leukocyte adhesion after liver transplantation.
Reperfusion injury involving oxygen radicals, leukocyte adhesion, and Kupffer cell activation has been suggested to contribute to the failure of transplanted livers. The aim of this study was to evaluate Kupffer cell activity, leukocyte adhesion, and the effect of the calcium channel blocker nisoldipine after rat liver transplantation by means of in vivo fluorescence microscopy to further investigate the mechanism of graft failure. Inclusion of 1.4 microM nisoldipine to the University of Wisconsin cold storage solution (UW) did not improve sinusoidal perfusion and vasoconstriction after transplantation compared with UW alone (82.7 +/- 1.0% vs. 79.2 +/- 1.7% perfused sinusoids; 7.3 +/- 0.1 vs. 8.0 +/- 0.2 microns diam of sinusoids; means +/- SE). Permanent as well as temporary adhesion of leukocytes rose from 9.4 +/- 0.8 and 10.2 +/- 0.5% in sham-operated controls to 19.1 +/- 2.2 and 19.2 +/- 0.5% after liver transplantation, respectively. Inclusion of the calcium channel blocker reduced permanent (9.1 +/- 0.8%; P < 0.05) and temporary adherent leukocytes (11.3 +/- 1.0%; P < 0.05). Phagocytosis of latex beads by Kupffer cells or other phagocytic cells as a function of activity rose after transplantation (e.g., periportal area: 509 +/- 44/mm2) compared with controls (316 +/- 22/mm2). This was significantly reduced by inclusion of nisoldipine to UW (322 +/- 32/mm2). The results of this study demonstrate activation of Kupffer cells and increase of leukocyte adhesion to the sinusoidal endothelial wall during reperfusion of transplanted livers. A calcium-dependent release of mediators by Kupffer cells that promote leukocyte adhesion is suggested as an underlying mechanism.
Animals↗
Comparative effects of crystalloid and small volume hypertonic hyperoncotic fluid resuscitation on hepatic microcirculation after hemorrhagic shock.
Hepatic microcirculation, leukocyte-endothelial interaction, and sinusoidal widths were studied by means of intravital microscopy in a non-heparinized fixed pressure hemorrhagic shock model in the rat. Asanguineous resuscitation was performed either with "adequate" amounts of lactated Ringer's solution (threefold shed volume/30 min) or 4 ml/kg/3 min 7.2% saline/10% Dextran 60 (HSDex) or 4 ml/kg/3 min 7.2% saline/10% hydroxyethylstarch 200/0.62 (HSHes). Hemorrhagic shock and resuscitation was paralleled by significant (P < 0.01) lumenal narrowing of sinusoids that remained largely uninfluenced by the type of fluid used for resuscitation (HSDex: 9.28 +/- 0.56; HSHes: 8.93 +/- 0.29, LR: 8.87 +/- 0.6 microns compared to 12.17 +/- 0.24 microns in controls). Whereas HSHes and LR-therapy resulted in comparably increased leukocyte adhesion to the sinusoidal wall, the dextran-containing solution led to a significant attenuation of leukocyte-endothelial interaction, suggesting involvement of dextran-binding adhesion molecules, e.g., selectins.
Animals↗
Ultrastructural correlates of liver graft failure from storage injury: studies of graft protection by Carolina rinse solution and pentoxifylline.
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Adenosine↗
Leukocyte-endothelial cell interactions in the liver after hemorrhagic shock in the rat.
Leukocyte-endothelial cell interactions in rat livers were investigated using intravital fluorescence microscopy following hemorrhagic shock (MAP at 40 mm Hg for 60 min) and resuscitation. Thirty minutes after resuscitation, when MAP was higher than 100 mm Hg, sinusoidal perfusion was only slightly reduced (>90% of controls). Firm adhesion of leukocytes increased to 370 +/- 54 leukocytes/mm2 after shock and resuscitation compared to control animals (48 +/- 8/mm2; mean +/- SEM; P < .01). Leukocyte-endothelium adhesion was highest in the portal areas and lowest in midzonal and pericentral regions (relationship:2.0: 1.1:1.0). Pretreatment with dexamethasone (5 mg/kg bw) resulted in a dramatic rise of adherent leukocytes following hemorrhagic shock (920 +/- 62/mm2; P < .001). Pretreatment with ibuprofen (15 mg/kg bw) resulted in a similar increase of adherent leukocytes after hemorrhagic shock (750 +/- 60/mm2; P < .001), while pretreatment with MK 886(10 mg/kg), inhibitor of lipoxygenase pathway, reduced leukocyte adhesion slightly (270 +/- 38/mm2). The results reveal that leukotrienes, e.g., released by activated macrophages, are involved in the regulation of leukocyte adhesion in liver sinusoids following hemorrhagic shock and resuscitation. The negative effect of dexamethasone and ibuprofen on hepatic leukocyte adhesion, however, has to be considered for therapeutic use.
Animals↗
The impact of liver preservation in HTK and UW solution on microcirculation after liver transplantation.
Severe microcirculatory disturbances due to endothelial cell damage and leukocyte adherence during reperfusion of transplanted livers are considered to contribute to early graft failure. Since the degree of reperfusion injury after liver transplantation depends on the length of preservation time and the solution used for preservation, the aim of our study was to assess three solutions with respect to microvascular perfusion and leukocyte adhesion. Therefore, rat livers were stored up to 24 h in Euro-Collins (EC), University of Wisconsin (UW), or histidin-tryphtophan-ketoglutarate (HTK) solutions prior to orthotopic transplantation. The livers were studied in situ 60 min postoperatively using intravital fluorescence video microscopy. Using simple syringe flushing (10 ml), sinusoidal perfusion decreased below 50% in EC preserved livers after 8 h preservation, in HTK preserved livers after 16 h preservation, and remained higher than 70% in livers preserved in UW up to 24 h. Permanent adhesion of leukocytes was increased more rapidly in organs after 1, 8, 16, and 24 h preservation in HTK (16%, 15%, 34%, and 49.7% +/- 4.7%) compared to those preserved in UW (15%, 18%, 17%; and 32.7% +/- 3.3%; P<0.05). Using a 10-fold volumn of the organ weight of HTK solution during the harvesting procedure, with an 8 min equilibration period, sinusoidal perfusion (39.6 +/- 4.7%) and leukocyte adhesion (42.7 +/- 3.1%) were not improved after 24 h. In contrast, equilibration with a volumn of approximately 40-times the liver weight improved sinusoidal perfusion (70.8% +/- 2.7%; P < 0.01) and leukocyte adhesion (24.9% +/- 3.1%; P < 0.01) significantly. Thus, using HTK solution, simple flushing prior to long-term cold storage resulted in microcirculatory disturbances when compared to UW solution. Larger volumns of HTK solution with an additional equilibration period of 8 min, however, reduced leukocyte adhesion and improved sinusoidal perfusion to a similar degree as UW solution.
Adenosine↗
Improvement of liver preservation by the calcium channel blocker nisoldipine. An experimental study applying intravital microscopy to transplanted rat livers.
It has been shown recently that inclusion of the calcium channel blocker nisoldipine to University of Wisconsin (UW) solution significantly improves survival after rat liver transplantation. To further elucidate the mechanisms involved, rat livers were stored for 1 h in UW solution with or without the addition of 1.4 microM nisoldipine (Miles, West Haven, Conn., USA). The liver grafts were investigated in vivo 90 min after transplantation by intravital fluorescence microscopy. Sinusoidal perfusion was reduced in all sublobular regions of the liver in the UW group (e.g. portal area: 76.7 +/- 2.1%) and in the nisoldipine group (85.8 +/- 1.5%). Diameters of liver sinusoids were comparably reduced in the UW and nisoldipine groups indicating that nisoldipine did not cause vasodilatation. Adhesion of leukocytes, however, rose significantly after liver transplantation particularly in periportal regions (25.8 +/- 2.5%) compared to controls (17.1 +/- 2.8%; P < 0.05). Adhesion of leukocytes was reduced when nisoldipine was included in UW solution (13.3 +/- 1.7%; P < 0.05). Administration of latex particles, which were given in additional experimental groups, demonstrated an impressive increase in phagocytic activity of Kupffer cells after liver transplantation in periportal and pericentral areas (161 +/- 14% and 184 +/- 19% of controls). Phagocytosis was significantly reduced by nisoldipine in the periportal region (101 +/- 10%; P < 0.01). Thus, the beneficial effect of nisoldipine was most pronounced in periportal regions, where the majority of Kupffer cells are located and leukocyte adhesion was at a maximum.
Adenosine↗
Reduction by superoxide dismutase of leukocyte-endothelial adherence after liver transplantation.
One hour after orthotopic rat liver transplantation, hepatic microcirculation and adhesion characteristics of leukocytes to the endothelial wall were studied with intravital microscopy. Cold storage for 1 and 8 hours in Euro-Collins solution resulted in reduction of perfused sinusoids to 83% and 48% and a decrease of leukocyte velocity from 417 microns/sec in controls to 311 microns/sec and 269 microns/sec, respectively. Additionally, the number of permanently adherent leukocytes rose from 4% in controls to 33% and 43% after cold storage for 1 and 8 hours. Intravenous injection of the free radical scavenger human recombinant superoxide dismutase (40 mg/kg) during reperfusion resulted in marked improvement of the hepatic microcirculation after both 1 and 8 hours of cold storage (91% and 69% perfused sinusoids; 420 microns/sec and 350 microns/sec leukocyte velocity; p less than 0.05). Furthermore, the percentage of permanently adherent leukocytes decreased to 13% and 28% after 1 and 8 hours of cold ischemia, respectively. These results support the hypothesis that oxygen-derived free radicals contribute to leukocyte adherence and microcirculatory failure after cold liver ischemia and transplantation. Thus, application of oxygen free radical scavengers during liver transplantation procedures might be useful to improve graft function.
Animals↗
Microcirculatory disturbances and leucocyte adherence in transplanted livers after cold storage in Euro-Collins, UW and HTK solutions.
Integrity of the hepatic microcirculation and maintenance of endothelial cell viability are critical components in preventing primary non-function after liver transplantation. Therefore, hepatic microcirculation and leucocyte-endothelial interaction were studied in rat livers stored for 1 h in Euro-Collins (EC), University of Wisconsin (UW), and histidine-tryptophan-ketoglutarate (HTK) solutions and subsequently transplanted. One hour after transplantation surgery, the livers were exposed under an intravital fluorescence microscope. After injection of the leucocyte marker acridine orange (1 mumol/kg), six pericentral fields were observed for 30 s and experiments were recorded continuously. The percentage of perfused sinusoids was reduced in the livers in the EC group (82.9%) in contrast to the UW (93.2%) and HTK groups (91.0%). Livers in the EC group showed a reduction in the diameters of pericentral sinusoids (7.3 +/- 0.2 microns; mean +/- SEM) compared with the UW group (9.5 +/- 0.2 microns; P less than 0.05) and HTK group (10.2 +/- 0.8 microns; P less than 0.05), indicating substantial cell swelling in livers stored in EC solution. Permanent adherence of leucocytes was most frequently observed in the EC group (33.5 +/- 1%), while this phenomenon was less pronounced in the UW group (14.5 +/- 1.1%; P less than 0.05) and HTK group (16.3 +/- 0.7%; P less than 0.05). Conversely, temporary adherence of leucocytes was reduced in the EC group (19.7 + 1.3%) compared with the UW group (30.5 + 2.1%) and the HTK group (34.4 + 0.8%).(ABSTRACT TRUNCATED AT 250 WORDS)
Adenosine↗
Methyl palmitate prevents Kupffer cell activation and improves survival after orthotopic liver transplantation in the rat.
The purpose of this study was to determine whether prevention of Kupffer cell activation following orthotopic liver transplantation improves postoperative survival. First, particle phagocytosis by Kupffer cells was monitored continuously from the uptake of colloidal carbon by the perfused liver. Unstored livers took up carbon at rates of around 150 mg/g per hour, whereas storage for 24 h in Euro-Collins solution nearly doubled values to about 290 mg/g per hour. Treatment of rats with methyl palmitate, an inhibitor of phagocytosis by Kupffer cells, reduced carbon uptake to about one-third to one-half of control values in unstored and stored livers, respectively. Oxygen uptake, which was increased about 25% in stored and unstored livers by infusion of colloidal carbon, was only increased 5%-10% in both groups following treatment with methyl palmitate, suggesting that Kupffer cell activation was prevented by methyl palmitate. In livers transplanted after storage for 6 h in Euro-Collins solution (nonsurvival conditions), control rats survived only about 12 h, while treatment with methyl palmitate increased survival time significantly--more than threefold--to about 40 h. These data are consistent with the hypothesis that activation of Kupffer cells following cold ischemic storage and reperfusion is an early event involved in liver graft failure.
Animals↗
Leukocyte adhesion and cell death following orthotopic liver transplantation in the rat.
The purpose of these experiments was to employ video microscopy to identify early pathological changes after orthotopic liver transplantation in the rat. Liver transplantation was performed using the cuff technique. Survival was greater than 90% when livers were stored for 1 hr in Ringer's solution prior to transplantation (survival conditions), whereas all rats died following storage of grafts for 4 hr in cold Euro-Collins solution (nonsurvival conditions). Postoperatively, each recipient animal was anesthetized, the abdomen was opened, and the liver was placed on the stage of an inverted fluorescence microscope equipped with a low-light ISIT video camera. Precautions were taken to prevent the liver surface from drying. The fluorescent dyes fluorescein sodium (1.0 mumol/kg), acridine orange (2.5 mumol/kg), and propidium iodide (1 mumol/kg) were injected intravenously to label hepatocytes, polymorphonuclear leukocytes, and the nuclei of irreversibly damaged cells, respectively. In livers from untransplanted rats, movement of labeled leukocytes through the hepatic sinusoids was smooth and rapid (velocity, 500-550 microns/sec) and margination (adhesion) of cells was minimal (less than 1%). After transplantation, however, velocity was diminished 2-3-fold, and margination was increased to 10% of leukocytes in survival groups and to 40% in nonsurvival groups 4 hr postoperatively. In the nonsurvival groups, irreversible cell death detected by propidium iodide fluorescence was minimal 15 min after transplantation--however, massive cell damage was detected 4 hr postoperatively. In addition, serum transaminases and necrosis were higher at 4 hr than 15 min postoperatively. Taken together, these data demonstrate that leukocyte margination increases following orthotopic liver transplantation and is followed rapidly by cell death. These events likely play a role in the mechanism of early graft failure following transplantation.
Animals↗
Carolina rinse solution--a new strategy to increase survival time after orthotopic liver transplantation in the rat.
Recently, we described a new solution, Carolina rinse, that prevents nonparenchymal cell injury in vitro after reperfusion of livers stored in University of Wisconsin cold solution (Currin RT, Toole JG, Thurman RG, Lemasters JJ. Transplantation 1990; 50: 1076). The present study was designed to examine the effect of Carolina rinse on graft survival in vivo. Unlike UW cold storage solution, which is high in potassium, Carolina rinse contains extracellular inorganic ions at levels similar to blood, a calcium channel blocker and a radical scavenger. Carolina rinse also contains fructose and mildly acidotic pH to reduce hypoxic cell death. Livers from Lewis rats were explanted, stored in UW cold storage solution under nonsurvival conditions, and rinsed with either 15 ml of Ringer's, UW solution, Carolina rinse, or Carolina rinse saturated with nitrogen prior to completion of implantation surgery. In the Ringer's rinse group, only 4% of recipients survived 30 days postoperatively. In this group, SGOT levels reached maximal values of about 5000 U/L. Survival was also poor (25%) when grafts were rinsed with UW solution. In the Carolina rinse group, however, 9 of 16 rats (56%) survived indefinitely, and maximal postoperative SGOT levels were reduced 3-fold. Liver injury indexed histologically was also decreased about 3-fold by Carolina rinse compared with the control group rinsed with Ringer's solution. Carolina rinse diminished postoperative sinusoidal endothelial cell damage assessed by electron microscopy and reduced carbon particle phagocytosis due to Kupffer cells significantly. Moreover, Carolina rinse diminished graft swelling and improved postoperative hepatic microcirculation compared with the Ringer's rinse group. Taken together, these results indicate that Carolina rinse is a superior alternative to Ringer's solution in vivo to protect liver grafts from reperfusion injury when removing high-potassium-containing cold storage solutions clinically prior to implantation.
Adenosine↗