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C Lehmann

Publications and source records attributed to C Lehmann.

At least 37 records · Page 2Linked to original sources
PubMed2001

Effects of iloprost, a stable prostacyclin analog, on intestinal leukocyte adherence and microvascular blood flow in rat experimental endotoxemia.

OBJECTIVE: To investigate the effects of iloprost, a stable prostacyclin analog, on leukocyte adherence in intestinal venules and intestinal microvascular blood flow in experimental endotoxemia. DESIGN: Prospective, randomized, controlled animal study. SETTING: Experimental laboratory. SUBJECTS: Twenty-one male Wistar rats weighing 190 +/- 40 g. INTERVENTIONS: The rats were divided equally into three groups: the first was a control group; the second received endotoxin (20 mg/kg lipopolysaccharide from Escherichia coli O55:B5 intravenously); and the third received endotoxin and intravenous iloprost infusion (2 ng.kg-1.min-1). MEASUREMENTS AND MAIN RESULTS: The distal small intestine of the animals was examined by using intravital fluorescence videomicroscopy 2 hrs after endotoxin challenge. Leukocytes were stained in vivo by means of rhodamine 6G. Intestinal microvascular blood flow was measured by laser Doppler flowmetry in the terminal ileum. Iloprost treatment significantly attenuated the count of adherent leukocytes in collecting venules (control, 61 +/- 10 n/mm2; lipopolysaccharide, 364 +/- 60 n/mm2; iloprost, 232 +/- 29 n/mm2; p <.05) and in postcapillary venules (control, 96 +/- 14 n/mm2; lipopolysaccharide, 470 +/- 21 n/mm2; iloprost 390 +/- 41 n/mm2; p <.05). Intestinal microvascular blood flow was decreased significantly in the lipopolysaccharide group (-49%), whereas iloprost-treated animals showed no significant difference compared with the control group. CONCLUSIONS: The study demonstrated that administration of iloprost attenuated leukocyte adherence in postcapillary and collecting intestinal venules and improved intestinal microvascular blood flow. Thus, iloprost treatment may impact endotoxin-induced intestinal injury.

Analysis of Variance↗
PubMed2001

Gastrointestinal development in the Drosophila embryo requires the activity of innexin gap junction channel proteins.

Cell to cell communication plays an essential role during pattern formation and morphogenesis of the diverse tissues and organs of the body. In invertebrates, such as the fruitfly Drosophila, the direct communication of closely apposed cells is mediated by gap junctions which are composed of oligomers of the innexin family of transmembrane channel proteins. Few data exist about the developmental role of the eight innexin genes which have been found in the Drosophila genome. We have investigated the role of the innexin 2 and ogre genes during gastrointestinal development of the fly embryo. Our findings suggest that innexins are involved in the formation of the proventriculus, an organ that develops at the foregut/midgut boundary by migration of primordial cells and subsequent infolding of epithelial tissue layers.

Animals↗
PubMed2000

Impaired binding of perforin on the surface of tumor cells is a cause of target cell resistance against cytotoxic effector cells.

Exocytosis of perforin, subsequent binding of perforin to the target cell membrane, and formation of lytic pores form an important pathway involved in the induction of tumor cell death by cytotoxic effector cells. Here we describe a novel escape mechanism employed by tumor cells to protect themselves from granule-mediated cell death: We were able to demonstrate that the resistance of the human leukemia cell line ML-2 to natural killer (NK)-cell-mediated killing is not caused by impaired NK-cell activation but by resistance against effector molecules contained in the granules of cytotoxic cells. No resistance was observed against other pore-forming agents like complement and streptolysin O. By using the NK-susceptible leukemia cell line K562, we could show that the induction of cell death by cytotoxic granules can be blocked completely by anti-perforin antibodies, indicating that perforin is essentially involved in this process. Flow cytometric data revealed that an impaired binding of perforin on the tumor cell membrane is mainly responsible for target cell resistance, because perforin turned out to bind well on K562 cells but is not able to attach to the surface of ML-2 cells. After impaired binding of perforin was identified as a potential mechanism of tumor cell resistance, leukemia cells from 6 patients with acute myeloid leukemia (AML) were examined. As predicted, AML cells that failed to bind perforin on their surface demonstrated complete resistance toward NK-cell-mediated cytotoxicity. Thus, perforin resistance could represent an important tumor escape mechanism that should be considered when cytotoxic effector cells are used for cellular immunotherapy. (Blood. 2000;96:594-600)

Bacterial Proteins↗
PubMed2000

Two-dimensional gel analysis of the proteome of lager brewing yeasts.

Modern lager brewing yeasts used in beer production are hybrid strains consisting of at least two different genomes. To obtain information on the identity of the parental strains that gave rise to industrial lager yeasts, we used two-dimensional (2-D) gel electrophoresis and analysed the proteomes of different Saccharomyces species isolated from breweries. We found that the proteome of lager brewing yeasts and of the type strains of S. carlsbergensis, S. monacensis and S. pastorianus can be interpreted as the superimposition of two elementary patterns. One originates from proteins encoded by a S. cerevisiae-like genome. The other corresponds to a divergent Saccharomyces species whose best representative is a particular S. pastorianus strain, NRRL Y-1551. A map of industrial lager brewing yeasts has been established, with the individual origin of proteins and with identification of protein spots by comparison to known S. cerevisiae proteins. This 2-D map can be accessed on the Lager Brewing Yeast Protein Map server through the World Wide Web. This study provides the first example of the use of proteome analysis for investigating taxonomic relationships between divergent yeast species.

Amino Acid Sequence↗
PubMed2000

TNF-alpha and IL-1alpha induce apoptosis in subconfluent rat mesangial cells. Evidence for the involvement of hydrogen peroxide and lipid peroxidation as second messengers.

Apoptosis of mesangial cells (MC) plays a role in glomerulonephritis (GN). In this study we investigated cytokine-induced apoptosis of cultured rat MC by morphological and biochemical features. TNF-alpha and IL-1alpha induced apoptosis in rat MC in a time- and concentration-dependent fashion. RT-PCR experiments revealed that MC express the TNF-receptor 1 (p60) gene constitutively. TNF-alpha as well as IL-1alpha stimulated the production of reactive oxygen species (ROS) and induced lipid peroxidation. Coincubation with catalase inhibited TNF-alpha and IL-1alpha induced apoptosis as well as lipid peroxidation. TNF-alpha, but not IL-1alpha increased the expression of c-jun. These results provide evidence that TNF-alpha and IL-1alpha induce apoptosis in rat MC with hydrogen peroxide and lipid peroxidation as second messengers. Increased c-jun expression may be a downstream intracellular signal of TNF-alpha-, but not IL-1alpha-induced apoptosis.

Animals↗
PubMed2000

Effects of the stable prostacyclin analogue iloprost on the plasma disappearance rate of indocyanine green in human septic shock.

OBJECTIVES: To evaluate the effect of the stable prostacyclin analogue iloprost on the plasma disappearance rate of indocyanine green (PDR) in patients with septic shock. DESIGN AND SETTING: A prospective clinical study in a university hospital intensive care unit. PATIENTS AND INTERVENTIONS: 20 patients in septic shock. Patients received iloprost infusion (1 ng/kg per minute) for 24 h. MEASUREMENTS AND RESULTS: PDR was determined by a femoral arterial fiberoptic catheter before, 1, 6, and 24 h after start and 1 h after end of iloprost infusion. PDR increased significantly 24 h after start of iloprost infusion (baseline: 13.9 +/- 1.7% vs. 18.6 +/- 2.2%/min) and decreased 1 h after end of infusion (13.7 +/- 1.7%/min; p < 0.002). There was no change in pHi, cardiac index, mean arterial pressure, heart rate, central venous pressure, or intrathoracic blood volume index. CONCLUSION: Administration of the stable prostacyclin analogue iloprost significantly increases PDR, indicating improvement in liver function.

Adult↗
PubMed2000

Structured parent education in the management of childhood atopic dermatitis: the Berlin model.

Childhood atopic dermatitis (AD) is a common disease with the prevalence rates increasing. Its chronic course with frequent relapses puts a special burden on both children and their parents. To maximise positive long-term outcome in the management of AD it is important to support parents in dealing with the chronic condition of their child in addition to treating symptoms. In the present article, we describe in detail the goals, structure, and content of the Berlin education program for parents of children with AD. The program aims to contribute towards a comprehensive, family-oriented management of childhood AD. Its objective is to improve parent's self-management skills with regard to their child's disease and to positively impact the course of the disease as well as the family's quality of life. Medical, nutritional and psychological issues are covered in six group sessions which are conducted by a multiprofessional team of paediatricians, psychologists and dieticians. Preliminary data show that the program has a desirable effect on aspects of quality of life and coping.

Adult↗
PubMed2000

Influence of heparin and hirudin on endothelial binding of antithrombin in experimental thrombinemia.

OBJECTIVE: During the last decade, experimental and clinical evidence has accumulated that antithrombin (AT) exerts anti-inflammatory effects when given in high doses. Meanwhile, AT substitution has been shown to significantly increase prostacyclin release. However, the link between endothelial AT binding and anti-inflammatory AT effects remains to be established in vivo, although heparin has been shown to counteract anti-inflammatory AT effects. We hypothesized that the administration of heparin in endotoxin-challenged rats would decrease endothelial AT binding and systemic prostacyclin concentrations. DESIGN: Prospective, randomized, controlled experimental in vivo study. SETTING: Research laboratory of a university hospital. ANIMALS: Fifty-six Wistar rats. INTERVENTIONS: Baseline values of coagulation variables were measured in six animals. Forty of 50 Wistar rats in the study groups were given endotoxin (50 mg x kg(-1) iv) and were treated with saline (group LPS), AT (15 units x kg(-1) x hr(-1)) (LPS+AT), AT and heparin (80 IU x kg(-1) x hr(-1)), or AT and hirudin (0.12 mg x kg(-1) x hr(-1)); the other 10 received saline instead of endotoxin and were treated with AT alone. Before endotoxin application, a tracheostomy was performed, and venous and arterial catheters were inserted for blood sampling and infusion. MEASUREMENTS: Intravital endothelial AT binding was studied by using fluorescence isothiocyanate-marked antibodies during intravital microscopy of intestinal submucosal venules. Systemic prostacyclin, thrombin-AT complex, and fibrinogen concentrations were measured after 4 hrs. Intergroup differences were tested by Kruskal-Wallis analysis of variance on ranks. MAIN RESULTS: AT and AT + heparin were equally effective in inhibiting systemic procoagulant turnover as reflected by fibrinogen concentrations. Only the administration of AT + hirudin significantly prevented fibrinogen consumption (p < .05). In contrast with all other treatments, the administration of heparin significantly reduced intravital endothelial AT binding (p < .05). However, prostacyclin concentrations were similarly increased in all endotoxin-challenged study groups irrespective of the anticoagulatory treatment. CONCLUSIONS: There is evidence that heparin in contrast with hirudin prevents AT from being bound to the endothelial cell surface in this experimental model. Under low-dose AT substitution, systemic prostacyclin concentrations do not depend on whether heparin or hirudin is used for thrombin inhibition. These results support the view that heparin may counteract anti-inflammatory AT effects by keeping AT away from its endothelial binding sites; however, the results question the view that decreased endothelial prostacyclin release is solely responsible.

Animals↗
PubMed1999

Molecular modeling and design of regioselectively addressable functionalized templates with rigidified three-dimensional structures.

Extensive conformational analysis of a series of beta-alkyl substituted cyclopeptides-cyclo(Pro(1)-Xaa(2)-Nle(3)-Ala(4)-Nle(5)-Pro(6)-Xaa(7)- Nle(8)-Ala(9)-Nle(10)) and cyclo[Pro(1)-Xaa(2)-Nle(3)-(Cys(4)- Nle(5)-Pro(6)-Xaa(7)-Nle(8)-Cys(9))-Nle(10)] as well as their corresponding unsubstituted core structures cyclo(Pro(1)-Xaa(2)-Ala(3)-Ala(4)-Ala(5)-Pro(6)-Xaa(7)-Ala(8)-Ala(9)- Ala(10)) and cyclo(Pro(1)-Xaa(2)-Ala(3)-Cys(4)- Ala(5)-Pro(6)-Xaa(7)-Ala(8)-Cys(9)-Ala(10)) has been performed employing both the ECEPP/2 and the MAB force fields (Xaa = Gly, L-Ala, D-Ala, Aib, and D-Pro). Results show that (a) possible three-dimensional structures of the cyclo(Pro(1)-Gly(2)-Lys(3)-Ala(4)-Lys(5)-Pro(6)-Gly(7)-Lys(8)-Ala(9)- Lys(10)) molecule are not limited to a single extended "rectangular" conformation with all Lys side chains oriented at the same side of the molecule; (b) conformational equilibrium in monocyclic analogues obtained by replacements of conformationally flexible Gly residues for L-Ala, D-Ala, Aib, or D-Pro is not significantly shifted towards the target "rectangular" conformational type; and (c) introduction of disulfide bridges between positions 4 and 9 is a very powerful way to stabilize the target conformations in the resulting bicyclic molecules. These findings form the basis for further design of rigidified regioselectively addressable functionalized templates with many application areas ranging from biostructural to diagnostic purposes.

Amino Acid Sequence↗
PubMed1999

Telomerase protein rather than its RNA is the target of phosphorothioate-modified oligonucleotides.

Human telomerase is a ribonucleoprotein which uses its internal RNA moiety as a template for telomeric DNA synthesis. This enzyme is up-regulated in most malignant tumors and is therefore considered as a possible cancer target. Here we examined the effects of differently modified oligomers on telomeraseactivity from HL-60 cell extracts (TRAP-ezetrade mark assay). Phosphorothioate-modified oligonucleotides (PS-ODNs) inhibited telomerase activity at subnanomolar concen-trations and proved to be more efficient than peptide nucleic acids. In contrast to all the investigated oligomers, PS-ODNs were found to bind to the protein motif of telomerase called the primer binding site but poorly to its RNA. This is suggested by kinetic investigations demonstrating a competitive interaction of PS-ODNs and TS primer at the primer binding site. The K m value of the TS primer was 10.8 nM, the K i value of a 20mer PS-ODN was 1.6 nM. When the TS primer was PS-modified a striking increase in the telomerase activity was found which correlates with the number of phosphodiesters replaced. The K m value of a completely PS-modified TS primer was 0.56 nM. Based on these results the design of chimeric ODNs is proposed consisting of a 5'-PS-modified part targeting the primer binding site and a 3'-terminus part targeting the telomerase RNA.

Binding, Competitive↗
PubMed1999

Investigating the lysis of small-cell lung cancer cell lines by activated natural killer (NK) cells with a fluorometric assay for NK-cell-mediated cytotoxicity.

Activation of natural killer (NK) cells with interleukin-2 (IL-2) and IL-12 leads to an enhanced lysis of tumour cells. We investigated the ability of NK cells, with or without prior activation, to lyse a variety of small-cell lung cancer (SCLC) target cells. Specific lysis was measured with a fluorometric assay for NK-cell-mediated cytotoxicity: target cells were labelled with 3,3'-dioctadecyloxacarbocyanine, a green membrane dye. After co-incubation with NK cells, dead target cells were stained with propidium iodide, a red DNA dye that only penetrates dead cells. Of all eight SCLC cell lines tested, three were susceptible to lysis by non-activated NK cells, three were only susceptible to lysis by NK cells activated with IL-2 and IL-12 and two were not even susceptible to lysis by activated NK cells. The differences in target cell susceptibility showed no correlation with the expression of MHC-I on the surface of the target cells or with the expression of the adhesion molecules CD50, CD54, CD58 or CD102. Comparing the kinetics of the lysis of one SCLC cell line sensitive to non-activated NK cells and one sensitive only to activated NK cells, we found that maximum lysis of the former was obtained after 1 h, whereas significant lysis of the latter was only obtained after 4 h of incubation. This might be due to different mechanisms engaged in target cell lysis.

Carcinoma, Small Cell↗
PubMed1999

[Changes in homeostasis during surgical liver resection].

OBJECTIVES: To assess changes in haemostasis during liver resection and to discuss the indications for antifibrinolytic therapy. STUDY DESIGN: Open prospective study. PATIENTS: The study included 39 consecutive non-cirrhotic patients presenting for liver resection under portal triad clamping. METHOD: General anaesthesia was obtained with thiopentone, fentanyl, vecuronium and isoflurane. Transfusion scheme was standardized. Aprotinin (5,000 kIU.kg-1 BW) was administered in case of unexplained bleeding in the operative field. Coagulation pattern was assessed by routine tests and thrombelastrography before surgery, before portal triad clamping, 5 min after reperfusion and at completion of surgery. Patients requiring aprotinin intraoperatively were compared to others. RESULTS: In 32 patients no significant bleeding occurred. Their coagulation pattern was moderately changed and remained within the normal range. In seven patients severe bleeding occurred which was treated with aprotinin. Their coagulation tests were significantly modified, especially after reperfusion, associating an increase in aPTT, TT, FDP, DDim, r + k and a decreased platelet count. CONCLUSION: These changes were more in favour of a dilution coagulopathy or a DIC than hyperfibrinolysis. Therefore substitutive therapy with coagulation factors should be preferred to an antifibrinolytic agent. A systematic administration of the latter for liver resection in non-cirrhotic patients is debatable, considering the allergic risk (reoperation for cancer recurrence), thrombosis facilitation (pedicle clamping) and high cost.

Aged↗
PubMed1999

Inhibition of tumor necrosis factor-alpha release in rat experimental endotoxemia by treatment with the 21-aminosteroid U-74389G.

OBJECTIVE: To determine the effect of the 21-aminosteroid U-74389G on tumor necrosis factor (TNF)-alpha release in experimental endotoxemia. DESIGN: Prospective, randomized, controlled animal study. SETTING: Experimental laboratory. SUBJECTS: Twenty-one male Wistar rats weighing 190+/-40 g. INTERVENTIONS: The rats were divided equally into 3 groups: a) control; b) endotoxemia (5 mg/kg lipopolysaccharide [LPS] from Escherichia coli 055:B5); and c) endotoxemia and U-74389G administration 30 mins before (3 mg/kg) and 60 mins after (1.5 mg/kg) endotoxin challenge. MEASUREMENTS AND MAIN RESULTS: At 0, 120, and 240 mins, serum levels of TNF-alpha were measured using a specific rat TNF-alpha ELISA kit. U-74389G-treated endotoxemic animals showed significantly reduced TNF-alpha release 120 mins after endotoxin challenge (control, 2.5+/-2.1 pg/mL; LPS, 4041+/-871 pg/mL; U-74389G, 1627+/-474 pg/mL [p < .05]). Two hundred forty minutes after LPS administration, TNF-alpha levels decreased, whereas values in the untreated LPS group remained twice as high as those in the U-74389G group (LPS, 863+/-182 pg/mL; U-74389G, 369+/-54 pg/mL [p < .05]). CONCLUSIONS: The study demonstrated that administration of U-74389G, which has radical-scavenging and membrane-stabilizing properties, decreased TNF-alpha release during endotoxemia. Thus, 21-aminosteroids may lend themselves to evaluation in the treatment of septic states.

Analysis of Variance↗
PubMed1999

Cigarette smoking as a triggering factor of hidradenitis suppurativa.

BACKGROUND: Hidradenitis suppurativa is a chronic inflammatory skin disease involving the axillary, inguinal and anogenital regions and sometimes, in addition, the submammary or sacral areas. The etiology of this condition is unknown. OBJECTIVE: A matched-pair case-control study was performed to evaluate the influence of smoking habits on the manifestation of this disease. METHODS: Patients who had received surgical treatment for hidradenitis suppurativa in two dermatological centers completed a questionnaire dealing with family history, course of the disease and smoking habits. To form a randomized matched-pair control group, an equal number of patients admitted for various other skin diseases such as atopic dermatitis, varicose veins, skin tattoos, alopecia areata or melanoma was matched for sex and age and evaluated for smoking habits. Statistical analysis was performed by use of several chi2 tests in a cross-table setting. Moreover, a comparison to the expected smoking prevalence in Germany based on national statistics was performed. RESULTS: Out of 84 patients treated for hidradenitis suppurativa, 63 subjects (27 men, 36 women) completed the questionnaire. The rate of active cigarette smokers was 88.9% (56 patients), whereas 4 subjects (6.4%) had never smoked. 3 patients (4.8%) stated to be ex-smokers, but 2 of these had quit smoking only recently and after onset of the disease. The rate of smokers in the matched-pair control group was 46%. The significantly higher proportion of active smokers among patients with hidradenitis suppurativa can be expressed by an odds ratio of 9.4, the calculated 95% confidence interval was 3.7-23.7 (p < 0.001). The expected smoking prevalence in Germany was 26.7% according to national statistics. 73% of our patients had no family history of hidradenitis suppurativa whereas 27% reported at least one affected first-degree relative. CONCLUSION: From the exceedingly high rate of smokers among patients with this condition we conclude that cigarette smoking is a major triggering factor of hidradenitis suppurativa. Remarkably, the disease can be categorized as a smoking sequel that is neither of vascular nor neoplastic nature. Because familial occurrence was rather rarely reported, and because an environmental factor in the form of cigarette smoking appears to be of crucial importance to trigger the disease, we assume that the genetic basis of hidradenitis suppurativa is polygenic rather than mendelian. Smoking cessation should be encouraged particularly in patients with hidradenitis suppurativa although it is unknown whether this improves the course of the disease.

Adolescent↗
PubMed1999

A switch in the cellular localization of macrophage migration inhibitory factor in the rat testis after ethane dimethane sulfonate treatment.

Macrophage migration inhibitory factor (MIF), one of the first cytokines to be discovered, has recently been localized to the Leydig cells in adult rat testes. In the following study, the response of MIF to Leydig cell ablation by the Leydig cell-specific toxin ethane dimethane sulfonate (EDS) was examined in adult male rats. Testicular MIF mRNA and protein in testicular interstitial fluid measured by ELISA and western blot were only marginally reduced by EDS treatment, in spite of the fact that the Leydig cells were completely destroyed within 7 days. Immunohistochemistry using an affinity-purified anti-mouse MIF antibody localized MIF exclusively to the Leydig cells in control testes. At 7 days post-EDS treatment, there were no MIF immunopositive Leydig cells in the interstitium, although distinct MIF immunostaining was observed in the seminiferous tubules, principally in Sertoli cells and residual cytoplasm, and some spermatogonia. A few peritubular and perivascular cells were also labelled at this time, which possibly represented mesenchymal Leydig cell precursors. At 14 and 21 days, Sertoli cell MIF immunoreactivity was observed in only a few tubule cross-sections, while some peritubular and perivascular mesenchymal cells and the re-populating immature Leydig cells were intensely labeled. At 28 days after EDS-treatment, the MIF immunostaining pattern was identical to that of untreated and control testes. The switch in the compartmentalization of MIF protein at 7 days after EDS-treatment was confirmed by western blot analysis of interstitial tissue and seminiferous tubules separated by mechanical dissection. These data establish that Leydig cell-depleted testes continue to produce MIF, and suggest the existence of a mechanism of compensatory cytokine production involving the Sertoli cells. This represents the first demonstration of a hitherto unsuspected pattern of cellular interaction between the Leydig cells and the seminiferous tubules which is consistent with an essential role for MIF in male testicular function.

Animals↗
PubMed1999

[Controlled reperfusion of ischemic extremity musculature to prevent free radical induced lesions].

Tissue injury following reperfusion represents an essential problem of reconstructive vascular surgery. Pathogenetically toxic oxygen radicals are considered to play a pivotal role. Pharmacotherapeutical approaches are based particularly on antioxidants and vasodilators. However, a standardized regimen is not yet clinically introduced. In 48 adult Lewis-rats lower limb ischemia was induced by aortal cross-clamping. Following 3.5 hours of ischemia intravascular flushing perfusion via the distal aorta with a heparinized electrolyte solution (group B). Group C received additionally oxypurinol, group D alprostadil and group E sodium selenite into the flushing solution. At 4 hours recirculation was established. After 10 min, 30 min and 24 hours of reperfusion we determined lactate, creatine kinase, lactate dehydrogenase, urea, malondialdehyde and the laser Doppler flux. At the end of the experiments biopsies were taken from M. tibialis anterior. In comparison to control animals (group A) we observed an attenuation of reperfusion injury in the groups treated with flushing perfusion. Free oxygen radical reactions measured by malondialdehyde release were significantly reduced (30 min: A-209.1 +/- 45.4, B-127.3 +/- 36.9, C-113.2 +/- 14.1, D-99.6 +/- 24.5, E-123.6 +/- 11.2 mmol/l, p < 0.05). The laser Doppler flux measurements corresponded with the biochemical analyses (30 min: A-52.4 +/- 11.1, B-48.0 +/- 11.0, C-72.6 +/- 12.0, D-74.4 +/- 13.3, E-62.6 +/- 10.8% of baseline). Histologically, treatment with alprostadil (PGE1) and oxypurinol revealed superior results. Standardized intraarterial flushing perfusion with antioxidants and vasodilators reduces reperfusion injury. Clinical trials are urgently required to confirm the experimental findings and to optimize the therapy of extremity ischemia/reperfusion injury in humans.

Animals↗