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  • 1
    Electronic Resource
    Electronic Resource
    Prevention and therapy of the adult respiratory distress syndrome (1995)
    Springer
    Lung 173 (1995), S. 139-164 
    Details
    ISSN: 1432-1750
    Keywords: Adult respiratory distress syndrome ; Antiinflammatory therapy ; Vasodilator inhalation ; Surfactant application ; Artificial ventilation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The complex pathophysiology of adult respiratory distress syndrome (ARDS) makes preventive and therapeutic concepts difficult. Ample experimental evidence indicates that ARDS can be prevented by blocking systemic inflammatory agents. Clinically, only heparin, for inhibition of coagulation phenomena, is presently used among this array of approaches. Corticosteroids have not proven to be beneficial in ARDS. Alternative antiinflammatory agents are being proposed and are under current clinical investigation (e.g. indomethacin, acetylcysteine, αl-proteinase inhibitor, antitumor necrosis factor, interleukin 1 receptor antagonist, platelet-activating factor antagonists). Symptomatic therapeutic strategies in early ARDS include selective pulmonary vasodilation (preferably by inhaled vasorelaxant agents) and optimal fluid balance. Transbronchial surfactant application, presently tested in pilot studies, may be available for ARDS patients in the near future and may have acute beneficial effects on gas exchange, pulmonary mechanics, and lung hemodynamics; its impact on survival cannot be predicted at the present time. Strong efforts should be taken to reduce secondary nosocomial pneumonia in ARDS patients and thus avoid the vicious circle of pneumonia, sepsis from lung infection, and perpetuation of multiple organ dysfunction syndrome. Optimal respirator therapy should be directed to ameliorate gas-exchange conditions acutely but at the same time should aim at minimizing potentially aggravating side effects of artificial ventilation (barotrauma, O2 toxicity). Several new techniques of mechanical ventilation and the concept of permissive hypercapnia address these aspects. Approaches with extracorporeal CO2 removal and oxygenation are being used in specialized centers.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00175656
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  • 2
    Electronic Resource
    Electronic Resource
    Alveolar surfactant and adult respiratory distress syndrome (1993)
    Springer
    Journal of molecular medicine 71 (1993), S. 177-190 
    Details
    ISSN: 1432-1440
    Keywords: Adult respiratory distress syndrome ; Alveolar surfactant ; Surfactant phospholipids ; Surfactant apoproteins ; Surfactant inhibition ; Hyaline membranes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The adult respiratory distress syndrome (ARDS) is characterized by extended inflammatory processes in the lung microvascular, interstitial, and alveolar compartments, resulting in vasomotor disturbances, plasma leakage, cell injury, and complex gas exchange disturbances. Abnormalities in the alveolar surfactant system have long been implicated in the pathogenetic sequelae of this life-threatening syndrome. This hypothesis is supported by similarities in pulmonary failure between patients with ARDS and preterm babies with infant respiratory distress syndrome, known to be triggered primarily by lack of surfactant material. Mechanisms of surfactant alterations in ARDS include: (a) lack of surface-active compounds (phospholipids, apoproteins) due to reduced generation/release by diseased pneumocytes or to increased loss of material (this feature includes changes in the relative composition of the surfactant phospholipid and/or apoprotein profiles); (b) inhibition of surfactant function by plasma protein leakage (inhibitory potencies of different plasma proteins have been defined); (c) “incorporation” of surfactant phospholipids and apoproteins into polymerizing fibrin upon hyaline membrane formation; and (d) damage/inhibition of surfactant compounds by inflammatory mediators (proteases, oxidants, nonsurfactant lipids). Alterations in alveolar surfactant function may well contribute to a variety of pathophysiological key events encountered in ARDS. These include decrease in compliance, ventilation-perfusion mismatch including shunt flow due to altered gas flow distribution (atelectasis, partial alveolar collapse, small airway collapse), and lung edema formation. Moreover, more speculative at the present time, surfactant abnormalities may add to a reduction in alveolar host defense competence and an upregulation of inflammatory events under conditions of ARDS. Persistent atelectasis of surfactant-deficient and in particular fibrin-loaded alveoli may represent a key event to trigger fibroblast proliferation and fibrosis in late ARDS (“collapse induration”). Overall, the presently available data on surfactant abnormalities in ARDS lend credit to therapeutic trials with transbronchial surfactant administration. In addition to the classical goals of replacement therapy defined for preterm infants (rapid improvement in lung compliance and gas exchange), this approach will have to consider its impact on host defense competence and inflammatory and proliferative processes when applied in adults with respiratory failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00180100
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  • 3
    Electronic Resource
    Electronic Resource
    Acceleration of experimental diabetic retinopathy in the rat by omega-3 fatty acids (1996)
    Springer
    Diabetologia 39 (1996), S. 251-255 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetic retinopathy ; rat model ; omega-3 fatty acids.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Omega-3 fatty acids exert several important biological effects on factors that may predispose to diabetic retinopathy. Potential pathogenetic mechanisms include platelet dysfunction, altered eicosanoid production, increased blood viscosity in association with impaired cell deformability and pathologic leucocyte/endothelium interaction. Therefore, we tested whether a 6-month administration of fish oil (750 mg Maxepa, 5 times per week), containing 14 % eicosapentaenoic acid (EPA) and 10 % docosahexaenic acid, could inhibit the development of experimental retinopathy of the streptozotocin-diabetic rat. The efficiency of fish oil supplementation was evaluated by measuring EPA concentrations in total, plasma and membrane fatty acids and by measuring the generation of lipid mediators (leukotrienes and thromboxanes). Retinal digest preparations were quantitatively analysed for pericyte loss, and the formation of acellular capillaries. Omega-3 fatty acid administration to diabetic rats resulted in a twofold increase of EPA 20:5 in total fatty acids, and a reduction of the thromboxane2/3 ratio from 600 (untreated diabetic rats) to 50 (treated diabetic rats). Despite these biochemical changes, diabetes-associated pericyte loss remained unaffected and the formation of acellular, occluded capillaries was increased by 75 % in the fish oil treated diabetic group (115.1 ± 26.8; untreated diabetic 65.2 ± 15.0 acellular capillary segments/mm2 of retinal area). We conclude from this study that dietary fish oil supplementation may be harmful for the diabetic microvasculature in the retina. [Diabetologia (1996) 39: 251–255]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418338
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  • 4
    Electronic Resource
    Electronic Resource
    Acceleration of experimental diabetic retinopathy in the rat by omega-3 fatty acids (1996)
    Springer
    Diabetologia 39 (1996), S. 251-255 
    Details
    ISSN: 1432-0428
    Keywords: Diabetic retinopathy ; rat model ; omega-3 fatty acids
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Omega-3 fatty acids exert several important biological effects on factors that may predispose to diabetic retinopathy. Potential pathogenetic mechanisms include platelet dysfunction, altered eicosanoid production, increased blood viscosity in association with impaired cell deformability and pathologic leucocyte/endothelium interaction. Therefore, we tested whether a 6-month administration of fish oil (750 mg Maxepa, 5 times per week), containing 14% eicosapentaenoic acid (EPA) and 10% docosahexaenic acid, could inhibit the development of experimental retinopathy of the streptozotocin-diabetic rat. The efficiency of fish oil supplementation was evaluated by measuring EPA concentrations in total, plasma and membrane fatty acids and by measuring the generation of lipid mediators (leukotrienes and thromboxanes). Retinal digest preparations were quantitatively analysed for pericyte loss, and the formation of acellular capillaries. Omega-3 fatty acid administration to diabetic rats resulted in a twofold increase of EPA 20∶5 in total fatty acids, and a reduction of the thromboxane2/3 ratio from 600 (untreated diabetic rats) to 50 (treated diabetic rats). Despite these biochemical changes, diabetes-associated pericyte loss remained unaffected and the formation of acellular, occluded capillaries was increased by 75% in the fish oil treated diabetic group (115.1±26.8; untreated diabetic 65.2±15.0 acellular capillary segments/mm2 of retinal area). We conclude from this study that dietary fish oil supplementation may be harmful for the diabetic microvasculature in the retina.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418338
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  • 5
    Electronic Resource
    Electronic Resource
    Advantage of buffered solutions or automated capnometry in air-filled balloons for use in gastric tonometry (1997)
    Springer
    Intensive care medicine 23 (1997), S. 423-427 
    Details
    ISSN: 1432-1238
    Keywords: Key words Intramucosal pH ; Gastric tonometry ; Blood gas analyzer ; Automated capnometry ; Carbon dioxide ; Steady-state equilibration time
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: To test accuracy, reproducibility and time constants of pCO2 measurement with the tonometric technique, using different media for filling the silastic balloon (saline, phosphate buffer, citrate buffer, air) and employing different analyzer devices (ABL3, ABL330, Nova Stat 5, automated capnometry). Design: Comparative laboratory study of different tonometric techniques, measuring test solutions with known pCO2 values due to pre-equilibration with three different pCO2 concentrations. Setting: Clinical laboratory of a university hospital intensive care unit. Measurements and results: The use of saline, as suggested for routine tonometry, led to negative bias values throughout, i. e. underestimation of pCO2 values, the extent of which depended on the blood gas analyzer device employed. Registration of the equilibration kinetics showed that full equilibration demanded 90 min regardless of the environmental pCO2 level. Replacing saline by buffered electrolyte solutions resulted in a significant improvement of bias, but did not change the kinetics of pCO2 equilibration. The employment of air-filled balloons, combined with automated capnometry, led to very low bias values, approaching zero, for all pCO2 levels, along with excellent precision. Time constants of equilibration were dramatically reduced, with full equilibration being achieved within 12.5 min. Conclusions: Buffered electrolyte solutions are preferable to saline for achieving reliable pCO2 measurements in gastric tonometry. Air-filled balloons, combined with automated capnometry, present excellent accuracy and reproducibility together with short equilibration times, thus offering “on-line” monitoring of even rapid changes in environmental pCO2.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001340050351
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  • 6
    Electronic Resource
    Electronic Resource
    Assessment of intestinal tissue oxygenation: the canary sings – but was does the twitter tell us? (2000)
    Springer
    Intensive care medicine 26 (2000), S. 1025-1027 
    Details
    ISSN: 1432-1238
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001340051314
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  • 7
    Electronic Resource
    Electronic Resource
    Recovery from circulatory shock in severe primary pulmonary hypertension (PPH) with aerosolization of iloprost (1998)
    Springer
    Intensive care medicine 24 (1998), S. 631-634 
    Details
    ISSN: 1432-1238
    Keywords: Key words Primary pulmonary hypertension ; Pulmonary selective vasodilatation ; Right heart decompensation ; Low output failure ; Inhaled iloprost ; Prostacyclin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: The treatment of decompensated right ventricular failure with vasodilators is difficult due to reduced systemic pressure and/or ventilation/perfusion (V/Q) mismatch with hypoxemia. In a recent study we demonstrated that inhaled vasodilatory prostanoids may offer a new strategy to achieve pulmonary selective vasodilatation and improvement of right ventricular function. We applied this new approach to a patient with circulatory shock due to primary pulmonary hypertension (PPH), complicated by a pulmonary infiltrate, who did not tolerate intravenous prostacyclin. Design: Case report. Setting: Intensive Care Unit (ICU), Medizinische Klinik Gießen, Germany. Patient: A 45-year-old woman with PPH presenting with decompensated right heart failure (ascites, pleural effusion), circulatory shock and commencing renal and hepatic failure, despite maximum therapy including the use of catecholamines. Intervention: Intermittent inhalation of aerosolized iloprost, the stable analogue of prostacyclin, and comparison to inhaled nitric oxide (NO). Subsequent long-term therapy with aerosolized iloprost, 150 μg/day. Measurements and results: In response to inhaled iloprost, pulmonary arterial pressure (PAP) decreased from 65 to 61 mmHg, cardiac index (CI) increased from 1.25 to 1.85 l/min per m2, and pulmonary vascular resistance (PVR) decreased from 2416 to 1549 dyn/s per cm5 while inhaled NO decreased the PVR from 2280 to 1920 dyn/s per cm5 without a decrease in PAP. Both of these interventions increased the arterial pO2 but did not change the systemic arterial pressure. In contrast, intravenous prostacyclin was not tolerated, due to systemic side effects. During repeated inhalations with iloprost, the baseline hemodynamics and gas exchange improved dramatically and renal and liver functions normalized. During 1 year of continued therapy, the clinical status improved very much, concomitant with improved hemodynamics, and the patient has been taken off the transplantation list. Conclusions: Inhalation of aerosolized iloprost may offer a new life-saving strategy in near desperate cases of pulmonary hypertension in which intravenous prostacyclin cannot be applied due to severe side effects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001340050628
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  • 8
    Electronic Resource
    Electronic Resource
    Omega-oxidized leukotriene B4 detected in the broncho-alveolar lavage fluid of patients with non-cardiogenic pulmonary edema, but not in those with cardiogenic edema (1991)
    Springer
    Intensive care medicine 17 (1991), S. 1-6 
    Details
    ISSN: 1432-1238
    Keywords: Lung edema ; Acute respiratory distress syndrome ; Leukotrienes ; LTB4 ; Omega-oxidation products of LTB4 ; Broncho-alveolar lavage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Leukotriene (LT) generation has been implicated in the pathogenesis of the acure respiratory distress syndrome, ARDS. In the present study, we analysed broncho-alveolar lavage fluids of patients on mechanical ventilation because of ARDS (17 samples taken from 9 patients) or because of cardiogenic edema (8 samples taken from 6 patients) and of healthy volunteers (10 samples from different donors). LTs were separated as methylated and non-methylated compounds using different HPLC procedures, and were identified by chromatographic mobility, on-line UV-spectrum analysis and post HPLC immunoreactivity. In the lavage samples of the healthy volunteers and the patients with cardiogenic edema, no LTs were detected by these technicues (detection limit≃0.1–0.2 ng/ml lavage fluid). By contrast, in 15 out of 17 samples from patients with ARDS LTB4 or its metabolites 20-OH-LTB4 and 20-COOH-LTB4 were detected. The endproduct of omega-oxidation, 20-COOH-LTB4, represented the quantitatively predominant compound, detected in the range of 0.3–2.6ng/ml perfusate. We conclude that the chemotactic agent LTB4 may be involved in the amplification of inflammatory events encountered in ARDS, and that the oxidized metabolites of LTB4 are particularly suitable for monitoring lung leukotriene generation under conditions of neutrophil efflux and oxidative stress.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01708400
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  • 9
    Electronic Resource
    Electronic Resource
    A double-blind, randomized, placebo-controlled trial of n-3 fatty acid based lipid infusion in acute, extended guttate psoriasis (1993)
    Springer
    Journal of molecular medicine 71 (1993), S. 634-643 
    Details
    ISSN: 1432-1440
    Keywords: Psoriasis ; Lipid infusion ; n-3 fatty acids ; Neutrophil leukotriene generation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Twenty patients hospitalized for acute psoriasis guttata with a minimum 10% of body surface area involvement (range 10–90%) completed a 10-day trial in which they were randomly allocated to receive daily infusions with either an n-3 fatty acid based lipid emulsion [100 ml/day with 2.1 g eicosapentaenoic (EPA) and 21 g docosahexaenoic acid (DHA)] or a conventional n-6 lipid emulsion (EPA+DHA〈0.1 g/100 ml). The severity of disease was evaluated by scoring daily erythema, infiltration, and desquamation and by a subjective scoring of clinical manifestations offered by the patients. Leukotriene (LT) and platelet-activating factor (PAF) generation were investigated in ionophore-stimulated neutrophils obtained on days 0, 1, 3, 5, 10, and 40. Moderate improvement in clinical manifestations was noted in the n-6 group (changes in score systems between 16–25% from baseline within 10 days). In contrast, the severity of disease markedly decreased in all patients of the n-3 group, with improvements in all score systems ranging between 45% and 76% within 10 days (P〈0.05 for each variable). The difference in response to the two regimens was evident within 4–7 days after onset of lipid infusion. A more than ten fold increase in neutrophil EPA-derived 5-1ipoxygenase product formation (LTB5, its omega-oxidation products, non-enzymatic degradation products of LTA5 and 5-hydroxyeicosapentaenoic acid) was noted in the n-3 group but not in the n-6 group. Neutrophil PAF generation increased in the n-6 group but decreased in the n-3 group. In conclusion, modulation of eicosanoid metabolism by intravenous n-3 fatty acid supplementation appears to exert a rapid beneficial effect on inflammatory skin lesions in acute guttate psoriasis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00184491
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  • 10
    Electronic Resource
    Electronic Resource
    NO und alternative inhalative Therapieansätze bei pulmonaler Hypertonie (1997)
    Springer
    Der Internist 38 (1997), S. 453-460 
    Details
    ISSN: 1432-1289
    Keywords: Schlüsselwörter Stickstoffmonoxid ; ARDS ; Stickstoffmonoxid ; pulmonale Hypertonie ; NO ; ARDS ; NO ; pulmonale Hypertonie ; Pulmonale Hypertonie ; Stickstoffmonoxid ; ARDS ; Stickstoffmonoxid ; Prostaglandin ; ARDS ; Prostaglandin ; pulmonale Hypertonie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Zusammenfassung Gerade die hohe Letalität des Adult Respiratory Distress Syndrome (ARDS) und der schweren pulmonalen Hypertonie läßt sich nach neuen Behandlungsmethoden suchen, mittels derer möglichst selektiv eine pulmonale Vasodilatation und ein besserer Gasaustausch erzielt werden könnten. Daß Stickstoffmonoxid (NO), am besten inhalativ appliziert, hier eine therapeutische Option sein könnte, liegt nahe. Die vorliegende Arbeit gibt einen Überblick über die NO-Wirkungen und die leider erheblichen Nebenwirkungen im pulmonalen Bereich. Es wird aber auch auf andere Möglichkeiten hingewiesen, besonders auf Prostaglandine, die ebenfalls im c-GMP- und c-AMP-Signaltransduktionsweg bei der Modulierung des Tonus der glatten Gefäßmuskulatur wirksam eingesetzt werden können.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001080050057
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