Biomedical subjects

M Hensel

Publications and source records attributed to M Hensel.

At least 55 records · Page 3Linked to original sources

PubMed1999

[Forced opioid detoxification under general anesthesia--a new challenge for anesthetists and intensive care physicians].

Treatment of opioid addicts by means of competitive opioid receptor antagonists was developed at the University of Vienna in 1987 by Loimer and co-workers. They compared two withdrawal regimens: The short Opiate withdrawal using a staggered naloxone regimen and the rapid opiate detoxification during general anesthesia by means of high doses of naloxone. Based on the latter concept, various modifications have been developed world-wide using either naloxone or as an alternative, naltrexone, an antagonist available for oral administration only. However, there are considerable objections to opioid detoxification during general anasthesia. The main criticism is based an the supposedly unacceptable high risk:benefit-ratio, the higher costs, the lack of psycho-social support, and the lack of prospective studies. However, first results suggest that rapid detoxification procedures are more successful in decreasing relapse than methods which are based on psychiatric treatment alone. As sympathetic hyperfunction is common in rapid detoxification procedures using high doses of opioid receptor antagonists, it is essential to avoid severe autonomic imbalance with possible subsequent impairment of organ functions. To prevent those disturbances, general anesthesia plays an important role. So far, there is almost no information about such methods in the anesthesiological literature. In this article the clinical relevance of such methods is discussed summarizing both the available literature and our own experience and we conclude that rapid opioid detoxification under general anesthesia is a safe and efficient method to suppress withdrawal symptoms. This treatment may be of benefit in patients who particularly suffer from severe withdrawal symptoms and who have failed repeatedly to complete conventional withdrawal.

Anesthesia, General↗

PubMed1999

Pathogenicity island 2 mutants of Salmonella typhimurium are efficient carriers for heterologous antigens and enable modulation of immune responses.

The potential use as vaccine delivery system of Salmonella typhimurium strains harboring defined mutations in the sseC (HH104) and sseD (MvP101) genes, which encode putative effector proteins of the type III secretion system of Salmonella pathogenicity island 2, was evaluated and compared with that of the well-characterized aroA mutant strain SL7207 by using beta-galactosidase (beta-Gal) as a model antigen. When orally administered to immune-competent or gamma interferon-deficient (IFN-gamma-/-) BALB/c mice, both mutants were found to be highly attenuated (50% lethal dose, >10(9) bacteria). Both strains were also able to efficiently colonize and persist in Peyer's patches. Immunization with HH104 and MvP101 triggered beta-Gal-specific serum and mucosal antibody responses equivalent to or stronger than those observed in SL7207-immunized mice. Although immunoglobulin G2 (IgG2) serum antibodies were dominant in all groups, IgG1 was also significantly increased in mice vaccinated with MvP101 and SL7207. Comparable beta-Gal-specific IgA and IgG antibodies were detected in intestinal lavages from mice immunized with the different strains. Antigen-specific CD4(+) T-helper cells were generated after vaccination with all vaccine prototypes; however, responses were significantly more efficient when HH104 and MvP101 were used (P < 0.05). Significantly higher levels of IFN-gamma were produced by restimulated spleen cells from mice immunized with HH104 than from those vaccinated with the MvP101 or SL7207 derivatives (P </= 0.05). Interestingly, the three strains induced major histocompatibility complex class I-restricted CD8(+) cytotoxic T cells against beta-Gal; however, cytotoxic T-lymphocyte responses were significantly stronger after immunization with HH104 (P < 0.05). These novel S. typhimurium attenuated strains constitute promising delivery systems for vaccine antigens. The qualitative differences observed in the obtained responses with different carriers may be useful for those applications in which a targeted immunomodulation is required.

Animals↗

PubMed1999

Increased intrapulmonary oxygen consumption in mechanically ventilated patients with pneumonia.

Pulmonary oxygen consumption (V(O2)pulm) is believed to be increased in patients with lung infection. In the present study, VO2pulm was estimated from the difference between total oxygen consumption measured with indirect calorimetry (V(O2)cal) and oxygen consumption assessed with the reverse Fick method (V(O2)Fick). Seventy-five patients requiring mechanical ventilation were included, and were divided for analysis into two groups according to the existence (n = 41) or absence (n = 34) of pneumonia. V(O2)pulm was correlated with various parameters of impaired lung function. To assess the metabolic function of the lung, the differences in lactate and glucose concentrations at different arterial-mixed venous concentrations were determined and transpulmonary lactate flux as well as glucose flux was calculated. As compared with V(O2)pulm in patients without pneumonia (19.4 +/- 1.2 ml/ min/m2), V(O2)pulm was significantly increased in patients with pneumonia (50.7 +/- 1.7 ml/min/m2 (p < 0.001). For intrapatient measurements of V(O2)pulm, a sufficient reproducibility was achieved. V(O2)pulm increased with the lung injury score, number of afflicted lobes, venous admixture, the transpulmonary lactate flux, and the transpulmonary glucose flux, respectively. We speculate that the increased V(O2)pulm of infected lungs is due to different mechanisms, including increased oxidative metabolism by essentially extrapulmonary structures such as neutrophils and macrophages, as well as by changes in the metabolic function of lung tissue itself.

Blood Glucose↗

PubMed1998

Whole genome scan for habitat-specific genes by signature-tagged mutagenesis.

Large numbers of new open reading frames can be identified by whole genome sequencing of microbial genomes. Efficient new approaches are required to investigate the role of the putative genes, or to identify genes required in distinct habitats. The novel technique 'signature-tagged mutagenesis' allows the identification of individual mutants within complex pools of mutants. Large numbers of mutants can be analyzed in a parallel manner for negative phenotypes like loss of function or attenuation of virulence. Further analysis of mutations identified by a negative selection procedure can be performed by linking the position of the respective mutations to genes identified by whole genome sequencing of microbes.

Gene Expression↗

PubMed1998

The role of the Aspergillus fumigatus areA gene in invasive pulmonary aspergillosis.

The areA gene of Aspergillus nidulans is a positive-acting transcriptional factor required for the expression of genes involved in the utilization of a broad range of nitrogen sources other than ammonium and glutamine. We have investigated the role in pathogenesis of the corresponding gene (AfareA) of Aspergillus fumigatus, a causative agent of invasive pulmonary aspergillosis. Stable and unstable AfareA- strains were constructed and tested for altered virulence in mice on the basis of host survival, mixed infection experiments and genetic reversion studies. These showed that the AfareA gene contributes to, but is not essential for, virulence. Strains carrying extragenic mutations that partially suppress the AfareA- phenotype for growth on different nitrogen sources were tested for altered virulence in mixed infection studies. One of these was found to be more virulent than the parental AfareA- strain.

Animals↗

PubMed1998

Genes encoding putative effector proteins of the type III secretion system of Salmonella pathogenicity island 2 are required for bacterial virulence and proliferation in macrophages.

The type III secretion system of Salmonella pathogenicity island 2 (SPI-2) is required for systemic infection of this pathogen in mice. Cloning and sequencing of a central region of SPI-2 revealed the presence of genes encoding putative chaperones and effector proteins of the secretion system. The predicted products of the sseB, sseC and sseD genes display weak but significant similarity to amino acid sequences of EspA, EspD and EspB, which are secreted by the type III secretion system encoded by the locus of enterocyte effacement of enteropathogenic Escherichia coli. The transcriptional activity of an sseA::luc fusion gene was shown to be dependent on ssrA, which is required for the expression of genes encoding components of the secretion system apparatus. Strains carrying nonpolar mutations in sseA, sseB or sseC were severely attenuated in virulence, strains carrying mutations in sseF or sseG were weakly attenuated, and a strain with a mutation in sseE had no detectable virulence defect. These phenotypes were reflected in the ability of mutant strains to grow within a variety of macrophage cell types: strains carrying mutations in sseA, sseB or sseC failed to accumulate, whereas the growth rates of strains carrying mutations in sseE, sseF or sseG were only modestly reduced. These data suggest that, in vivo, one of the functions of the SPI-2 secretion system is to enable intracellular bacterial proliferation.

Acetyltransferases↗

PubMed1998

Hyperprocalcitonemia in patients with noninfectious SIRS and pulmonary dysfunction associated with cardiopulmonary bypass.

BACKGROUND: The incidence of noninfectious systemic inflammatory response syndrome (SIRS) associated with coronary artery bypass surgery and the potential role of several inflammatory parameters as early markers of pulmonary dysfunction induced by cardiopulmonary bypass (CPB) were investigated. METHODS: Forty patients undergoing elective coronary artery bypass surgery were studied prospectively. Perioperative lung function was monitored using the lung injury score introduced by Murray and colleagues, by measuring venous admixture (Qs/Qt), and, in some cases, by measuring extravascular lung water. Serum concentrations of the inflammatory parameters (procalcitonin, interleukin-6, sL-selectin, leukocyte elastase, neopterin, leukocyte counts, and C-reactive protein) were determined sequentially. The American College of Chest Physicians-Society of Critical Care Medicine classification system was used to diagnose SIRS. RESULTS: According to the entry criteria, SIRS developed in 17 (42%) patients after operation. Nine patients of this group showed signs of acute pulmonary impairment, whereas patients without SIRS had no lung injury. In all patients with acute lung injury, distinct increases in procalcitonin concentrations ranging from 5.1 to 14.3 ng/ml were measured. In patients with SIRS but without acute lung injury and in patients without SIRS, none or only negligible increases in serum concentrations of procalcitonin were seen. Compared with procalcitonin, other inflammatory parameters investigated were less sensitive and less specific to indicate pulmonary dysfunction secondary to CPB. CONCLUSIONS: Procalcitonin seems to be an appropriate parameter indicating the early development of severe noninfectious SIRS and for predicting pulmonary dysfunction secondary to CPB.

Aged↗

PubMed1998

Mutations in Salmonella pathogenicity island 2 (SPI2) genes affecting transcription of SPI1 genes and resistance to antimicrobial agents.

The Salmonella typhimurium genome contains two pathogenicity islands (SPI) with genes encoding type III secretion systems for virulence proteins. SPI1 is required for the penetration of the epithelial layer of the intestine. SPI2 is important for the subsequent proliferation of bacteria in the spleens of infected hosts. Although most mutations in SPI2 lead to a strong reduction of virulence, they have different effects in vitro, with some mutants having significantly increased sensitivity to gentamicin and the antibacterial peptide polymyxin B. Previously we showed that certain mutations in SPI2 affect the ability of S. typhimurium to secrete SPI1 effector proteins and to invade cultured eukaryotic cells. In this study, we show that these SPI2 mutations affect the expression of the SPI1 invasion genes. Analysis of reporter fusions to various SPI1 genes reveals highly reduced expression of sipC, prgK, and hilA, the transcriptional activator of SPI1 genes. These observations indicate that the expression of one type III secretion system can be influenced dramatically by mutations in genes encoding a second type III secretion system in the same cell.

Animals↗

PubMed1998

Parenteral selenium supplementation in critically ill patients--effects on antioxidant metabolism.

Decreased plasma selenium (Se) levels are common in critically ill patients. Oxidative stress is regarded as one possible cause of the Se deficiency. We investigated in 20 critically ill patients with decreased plasma selenium concentrations the antioxidant metabolism during parenteral selenium supplementation (week 1: 2 x 500 micrograms; week 2:1 x 500 micrograms, week 3:3 x 100 micrograms sodium selenite). As marker of oxidative stress we measured the plasma malondialdehyde levels on days 0, 1, 3, 7, 14, and 21. The content of reduced and oxidized glutathione as well as the leucocyte activity marker elastase were estimated on the same days. Initial plasma Se levels were considerably decreased (0.44 +/- 0.1 mumol/l, mean +/- SEM). After one day of supplementation Se concentrations were in the reference range. Plasma malondialdehyde levels and the ratio of oxidized and reduced glutathione were initially elevated and decreased beginning on day 3 of supplementation. The mean elastase level was 113 +/- 10 micrograms/l on day 0. On day 3 elastase values decreased significantly (85 +/- 13 micrograms/l, p < 0.05; day 21, 19 +/- 7 micrograms/l, p < 0.001). Antioxidant metabolism showed significant changes beginning after 72 hours of therapy. This latency may be explained with the induction of the enzyme glutathione peroxidase. The lowered plasma Se concentrations measured in the critically ill patients and the significant effects on antioxidant metabolism during supplementation emphasized the importance of selenium administration in these patients.

Adult↗

PubMed1997

Intracellular Ca2+ dependence of nitric oxide mediated enhancement of interleukin-8 secretion in human endothelial cells.

Nitric oxide (NO.) can induce transient [Ca2+] changes in endothelial cells not different from receptor mediated signalling. Whether this Ca2+ signal may provide a link with IL-8 secretion induced by NO. donors was investigated in human endothelial cells. Sodium nitroprusside (SNP) and S-nitroso-N-acetyl-DL-penicillamine (SNAP) dose dependently increased IL-8 production in this cell type. Additive IL-8 secretion was found with TNFalpha. Buffering intracellular Ca2+ with MAPT/AM suppressed NO. induced [Ca2+]i changes and reduced subsequent IL-8 secretion. The additive effect of both NO. donors on TNFalpha induced IL-8 secretion was completely blocked in the presence of MAPT/AM. SKF 96365, which has been shown to block receptor mediated Ca2+ entry, and TMB-8, which blocks intracellular Ca2+ release, both inhibited IL-8 secretion, particularly when TNFalpha was used as a costimulator, indicating that [Ca2+]i changes are important components of IL-8 induction by NO..

Calcium↗

PubMed1997

Nitric oxide induces transient Ca2+ changes in endothelial cells independent of cGMP.

Ca2+ changes induced by nitric oxide (NO.) were investigated in cultured human endothelial cells. Sodium nitroprusside (SNP) (1-100 mumol/L) and S-Nitroso-N-acetylpenicillamine (SNAP) (100 mumol/L) were used as NO. donors. The cytoplasmatic Ca2+ concentration was calculated using ratiometric FURA2 fluorescence measurements. Both NO. donors caused transient oscillatory Ca2+ changes, which were not detectable in the presence of oxyhemoglobin (50 mumol/L). Digital ratio imaging revealed initiation sites within cells where Ca2+ increases started spreading, which indicates that nonuniformly distributed targets might be involved in these reactions. Calcium was released from intracellular stores as indicated by experiments performed in Ca(2+)-free buffer. L-type Ca(2+)-channel blocker diltiazem (100 mumol/L) was not able to block these responses. NO.-induced Ca2+ release from intracellular stores caused capacitative Ca2+ entry. Both thapsigargin (1 mumol/L) and cyclopiazonic acid (10 mumol/L) inhibited the SNP response completely, whereas neither ryanodine (up to 100 mumol/L) nor dantrolene (100 mumol/L) was able to inhibit Ca2+ changes induced by SNP, indicating that primarily inositol 1,4,5-triphosphate (IP3)-dependent stores are released upon stimulation with NO.. A small inhibitory effect of ATP- and SNP-induced peak [Ca2+]i increase was measured in the presence of both caffeine (20 mmol/L) and procaine (1 mmol/L). Evidence is presented that cGMP is not involved in NO.-induced Ca2+ signals, as neither inhibitors of guanylate cyclase (methylene blue and LY 83583) nor cell permeant analogues of cGMP altered or simulated [Ca2+] changes. An inhibitor of cGMP-dependent protein kinase was also ineffective. We therefore propose that endothelial cells have specific targets proximal or at IP3 receptors to induce Ca2+ changes in endothelial cells stimulated with NO..

Adenosine Triphosphate↗

PubMed1997

Transient Ca2+ changes in endothelial cells induced by low doses of reactive oxygen species: role of hydrogen peroxide.

Cultured human and rat endothelial cells were used to study cellular toxicity and Ca2+ signalling upon exposure to reactive oxygen species. Superoxide and hydrogen peroxide (O2.-/H2O2) were produced by the hypoxanthine/xanthine oxidase system (HX/XO) and caused intracellular Ca2+ concentration ([Ca2+]i) to rise steadily when activities above 2 mU/ml were used. These Ca2+ increases were also measured when the glucose/glucose oxidase (G/GO) system above 5 mU/ml was used to produce hydrogen peroxide (H2O2). Gross morphological changes appeared to parallel elevated [Ca2+]i levels preceding cell death. However, when HX/XO or G/GO were used at non toxic doses rapid and transient changes in [Ca2+]i were measured. These treatments did not alter subsequent receptor mediated Ca2+ signalling induced by ATP (10 microM) or histamine (100 microM). Superoxide dismutase (50 U/ml), which dismutates O2.- into H2O2 also had no influence, whereas catalase (50 U/ml), which removes H2O2, completely diminished transient [Ca2+]i responses. H2O2 added directly was able to induce similar Ca2+ transients when concentrations of at least 500 microM were used. Buffering trace amounts of iron (o-phenanthroline; 200 microM) in order to inhibit .OH radical formation was not effective to alter Ca2+ changes. Experiments performed in Ca(2+)-free buffer showed a similar rise in [Ca2+]i and readdition of Ca2+ to the extracellular medium indicated the activation of store operated Ca2+ entry. Blocking Ca(2+)-ATPases of the endoplasmatic reticulum with thapsigargin (1 microM) inhibited ROS induced transient increases and cells preincubated with pertussis toxin (200 nM) showed unchanged Ca2+ transients after exposure to both enzyme systems. Phospholipase C inhibitor U73122 (2 microM) effectively reduced hydrogen peroxide induced emptying of intracellular stores. Taken together, we demonstrate that enzymatically produced non-toxic H2O2 rather than O2.- or .OH causes calcium signalling from thapsigargin sensitive stores, and activates store operated Ca2+ entry at least partially by activating phospholipase C. These changes clearly differ from pathological 'oxidative stress' associated with a progressive increase in [Ca2+]i.

Animals↗

PubMed1997

Functional analysis of ssaJ and the ssaK/U operon, 13 genes encoding components of the type III secretion apparatus of Salmonella Pathogenicity Island 2.

We have investigated the structure and transcriptional organization of 13 genes of Salmonella Pathogenicity Island 2 (SPI2) that encode components of the second type III secretion apparatus of Salmonella typhimurium. ssaK, L, M, V, N, O, P, Q, R, S, T, U constitute one operon of 10 kb. ssaJ lles upstream of ssaK and is the terminal gene of another operon. The deduced products of ssaJ, ssaK, ssaV, ssaN, ssaO, ssaQ, ssaR, ssaS, ssaT, and ssaU show greatest similarity to the Yersinia spp. genes yscJ, yscL, lcrD, yscN, yscO, yscQ, yscR, yscS, yscT, and yscU, respectively. The products of the ssaL, ssaM and ssaP genes do not have significant similarity to products of other type III secretion systems, and might be important for the specific function of the SPI2 type III secretion system. Bacterial strains carrying different ssa mutations display minor alterations in terms of serum sensitivity when compared with the wild-type strain, but none are defective in replication within macrophage-like RAW 264.7 cells. However, some of the ssa mutant strains invade HEp2 cells less efficiently and are less cytotoxic to RAW 264.7 macrophages than the wild-type strain. We show that the invasion defect is correlated with a lack of SipC in culture supernatants of these mutant strains. SipC is a product of the SPI1 type III secretion system of S. typhimurium, and is important for epithelial cell invasion. Therefore, mutations in SPI2 can affect the SPI1 secretion system, which raises the possibility of an interaction between the two type III secretion systems.

Amino Acid Sequence↗

PubMed1997

Management of swallowing disorders and chronic aspiration by glottic closure procedure.

We report an 18-year-old man with a posterior fossa tumor who had to undergo a partial resection of the tumor and supportive radiation therapy. Functional deficits of the lower cranial nerves, particularly the glossopharyngeal and vagal nerves, associated with severe swallowing disorders and refractory aspiration pneumonia were seen postoperatively. The admission to the intensive care unit (ICU) resulted from increasing respiratory failure accompanied by recurrent septic episodes. Nutritional support via nasogastric tube and later percutaneous endoscopic gastrostomy (PEG) were hampered by complications such as persistent sinusitis, local dermatitis surrounding the entrance of the PEG tube, and the development of duodenal ulcers. Furthermore, the use of continuous subglottic aspiration failed to prevent pulmonary infections. After a 9-week stay in the ICU due to inadequate antimicrobial therapy of aspiration pneumonia and the patient's persistent sepsis, a temporary surgical separation of airway and food passages was performed by glottic closure. Subsequently chronic aspiration stopped, and 3 months after admission to the ICU, the patient had stable vital organ function and was transferred to a surgical ward free of infections. Glottic closure was reversed successfully 7 months later. When compared with laryngeal function on admission, there was no more impairment. Thus, temporary glottic closure seems to be an efficacious treatment to prevent life-threatening septic complications in patients with refractory aspiration pneumonia.

Adolescent↗

PubMed1997

Analysis of the boundaries of Salmonella pathogenicity island 2 and the corresponding chromosomal region of Escherichia coli K-12.

We recently identified a pathogenicity island (SPI2) located at 30.7 centisomes on the Salmonella typhimurium chromosome. SPI2 contains genes encoding a type III secretion system whose function is distinct from that of the type III secretion system encoded by a pathogenicity island (SPI1) at 63 centisomes which is involved in epithelial cell entry. An analysis of the boundaries of SPI2 and comparison with the corresponding region of the Escherichia coli chromosome revealed that SPI2 inserted adjacent to the tRNA(Val) gene. The E. coli chromosome contains 9 kb of DNA at the region corresponding to the SPI2 insertion point which appears to be absent in S. typhimurium. The distribution of SPI1 and SPI2 was examined in various Salmonella isolates. In contrast to type III secretion system genes of SPI1, those of SPI2 are not present in Salmonella bongori, which diverged at the first branch point in the Salmonella lineage. These and other data indicate that SPI2 was acquired by a Salmonella strain already harboring SPI1 by horizontal transfer from an unknown source.

Base Sequence↗

PubMed1997

[Continuous "high flux" dialysis: an effective renal replacement therapy for intensive care patients].

Currently available replacement therapies for the treatment of acute renal failure are reviewed. Particular interest is focused on their application in intensive care, especially in septic patients. Underlying principles and mechanisms of action are explained. The continuous "High flux-dialysis" is shown to be a particularly effective form of renal replacement therapy.

Acute Kidney Injury↗

PubMed1996

Identification of a virulence locus encoding a second type III secretion system in Salmonella typhimurium.

Mapping the insertion points of 16 signature-tagged transposon mutants on the Salmonella typhimurium chromosome led to the identification of a 40-kb virulence gene cluster at minute 30.7. This locus is conserved among all other Salmonella species examined but is not present in a variety of other pathogenic bacteria or in Escherichia coli K-12. Nucleotide sequencing of a portion of this locus revealed 11 open reading frames whose predicted proteins encode components of a type III secretion system. To distinguish between this and the type III secretion system encoded by the inv/spa invasion locus known to reside on a pathogenicity island, we refer to the inv/spa locus as Salmonella pathogenicity island (SPI) 1 and the new locus as SPI2. SPI2 has a lower G+C content than that of the remainder of the Salmonella genome and is flanked by genes whose products share greater than 90% identity with those of the E. coli ydhE and pykF genes. Thus SPI2 was probably acquired horizontally by insertion into a region corresponding to that between the ydhE and pykF genes of E. coli. Virulence studies of SPI2 mutants have shown them to be attenuated by at least five orders of magnitude compared with the wild-type strain after oral or intraperitoneal inoculation of mice.

Animals↗

PubMed1996

[Changes in coagulation physiology and rheology after preoperative normovolemic hemodilution].

AIM: In a prospective randomised controlled trial the effect of preoperative normovolaemic haemodilution on coagulation, plasma viscosity and plasma protein levels was examined. METHOD: 50 patients undergoing gastrectomies were investigated (haemodilution group, n = 30; control group, n = 20). In the haemodilution group a haematocrit of 30% was aimed at. Blood was replaced by normovolaemic infusion of 6% hydroxyethyl starch 200/0.5. MAIN RESULTS: Haematocrit, colloid osmotic pressure, total serum protein, serum albumin and platelet count were significantly decreased intra- and postoperatively in the haemodilution group compared with control group (p < 0.01). All of these showed no differences between the two groups on the 7th postoperative day. Global coagulation parameters showed dilutional influences without significant differences between the two groups. Measurements of rheological parameters showed a statistically significant decrease in plasma viscosity in the haemodilution group compared with control group (p < 0.01). Haemodilution led to a marked reduction in the use of homologous blood (1 unit/haemodilution group; 10 units/ control group). The average volume of 6% hydroxyethyl starch 200/0.5 administered per patient was 15.2 ml/kgKM/d (7.6-22.2 ml/kgKM/d) in the haemodilution group and 12.7 ml/ kgKM/d (8.4-17.7 ml/kgKM/d) in the control group. CONCLUSION: Haemodilution induced decreases in plasma coagulation, platelet count and plasma proteins did not cause any functional impairement and may just reflect dilution of these parameters. It seems that infusion of 6% hydroxyethyl starch 200/0.5 in an amount of 10-20 ml/kgKM/d does not result in a relevant decrease in coagulation parameters.

Adult↗