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  • 1
    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
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  • 2
    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
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  • 3
    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
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 71 (1993), S. 177-190 
    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
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  • 5
    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
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Intensivmedizin und Notfallmedizin 36 (1999), S. 104-125 
    ISSN: 1435-1420
    Keywords: Key words Acute/adult respiratory distress syndrome ; nitric oxide ; prostacyclin ; surfactant ; mechanical ventilation ; liquid ventilation ; membrane oxygenation? ; Schlüsselwörter Acute/adult respiratory distress syndrome ; Stickstoffmonoxid ; Prostazyklin ; Surfactant ; mechanische Beatmung ; Liquidventilation ; extrakorporale Membranoxygenierung
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Diese Übersicht faßt die aktuell diskutierten Therapiestrategien beim ARDS vor dem Hintergrund ihrer klinischen Etablierbarkeit zusammen. Die vorgestellten Behandlungskonzepte reichen von antiinflammatorischen Therapieansätzen über Stickstoffmonoxid und Surfactant bis zu neuen Beatmungsstrategien.
    Notes: Summary This review summarizes actually discussed therapeutic strategies in ARDS and their possible role for clinical use. The presented therapeutic modalities include antiinflammatory treatment, nitric oxide and surfactant and new ventilation regimes.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Intensivmedizin und Notfallmedizin 37 (2000), S. 251-256 
    ISSN: 1435-1420
    Keywords: Key words¶Acute respiratory failure –¶acute respiratory distress syndrome (ARDS) –¶hypoxemic respiratory failure –¶lung edema –¶non-invasive ventilation (NIV) – pneumonia ; Schlüsselwörter¶Akutes Lungenversagen (ARDS) – Akute respiratorische Insuffizienz – Hypoxämisches respiratorisches¶Versagen – Lungenödem –¶Non-invasive Beatmung (NIV) – Pneumonie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die non-invasive Beatmung (NIV) ist als Alternative zur konventionellen mechanischen Beatmung bei akuter Exazerbation einer chronisch obstruktiven Lungenerkrankung (COPD) anerkannt. Im Gegenteil dazu ist der Stellenwert und die Effizienz der NIV bei Patienten mit akutem Lungenversagen bei anderer Genese als einer COPD noch unklar. Ziel dieser Übersicht ist es den Stellenwert der NIV für das akute hypoxämische Lungenversagen zu bestimmen.
    Notes: Summary Non-invasive ventilation (NIV) has been proposed as an efficient alternative to conventional mechanical ventilation during acute exacerbation of chronic obstructive pulmonary disease (COPD). In contrast, the value and benefit of NIV used in patients suffering from acute respiratory failure unrelated to COPD remain unclear. The objective of this overview is to determine the role of NIV in acute hypoxemic respiratory failure.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Intensivmedizin und Notfallmedizin 37 (2000), S. 671-673 
    ISSN: 1435-1420
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1435-1420
    Keywords: Key words Adult respiratory distress syndrome (ARDS) –¶alveolar surfactant –¶hyaline membranes –¶surfactant phospholipids –¶surfactant apoproteins surfactant inhibition ; Schlüsselwörter Acute Respiratory Distress Syndrome (ARDS) –¶Alveolärer Surfactant –¶Hyaline Membranen Surfactant ¶Phospholipide –¶Surfactant Apoproteine –¶Surfactant Inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Das akute Atemnotsyndrom (ARDS) ist durch ausgedehnte inflammatorische Prozesse im mikrovaskulären, interstitiellen und alveolären Kompartiment der Lunge charakterisiert. Dies führt zu vasomotorischen Veränderungen der pulmonalen Strombahn, Extravasation von Plasmaproteinen, Zellschädigung und schweren Gasaustauschstörungen. Ursächlich werden seit langem auch Veränderungen des alveolären Surfactant-Systems in der pathogenetischen Sequenz dieses lebensbedrohlichen Syndroms diskutiert. Diese Hypothese wird nicht zuletzt durch den ähnlichen Verlauf der respiratorischen Insuffizienz beim ARDS und bei Frühgeborenen (Infant Respiratory Distress Syndrome [IRDS]), bei denen ein primärer Surfactant-Mangel zugrunde liegt, unterstützt. Die Surfactant-Veränderungen beim ARDS umfassen: Mangel an oberflächenaktiven Substanzen, Veränderungen in der Surfactant-Komposition, Veränderungen in der relativen Surfactant-Subtypenverteilung, Inhibition der Surfactant-Funktion durch extravadierte Plasmaproteine sowie Inhibition oder Veränderung der Surfactant-Komponenten durch inflammatorische Mediatoren.¶   Diese Veränderungen der alveolären Surfactant-Funktion tragen zu den verschiedenen pathophysiologischen Merkmalen beim ARDS bei. Zentrale Bedeutung nehmen dabei der Verlust der Lungencompliance, Ventilations-Perfusions-Verteilungsstörungen einschließlich intrapulmonalem Shunt-Fluß aufgrund einer gestörten Ventilationsverteilung (Atelektasen, partieller Alveolarkollaps, Kollaps der kleinen Atemwege) und Lungenödembildung ein. Darüber hinaus scheinen persistierende Atelektasen, begünstigt durch Surfactant-Mangel und eine alveoläre Fibrinbeladung, Schlüsselreize für die Fibroblastenproliferation und die Ausbildung der Fibrose in der späten Phase der ARDS (Kollaps-Induration) zu sein.¶   Zusammenfassend scheinen die gegenwärtig verfügbaren Daten zu den Störungen der alveolären Surfactant-Funktion beim ARDS therapeutische Studien zur transbronchialen Surfactant-Applikation zu rechtfertigen. In zwei klinischen Untersuchungen, deren Ziel die Überprüfung der sicheren und effizienten Anwendbarkeit einer hohen Dosis transbronchial applizierten Surfactants bei ARDS Patienten war, konnte eine akute Verbesserung des Gasaustausches nachgewiesen werden. Begleitend zur Oxygenierungsverbesserung kam es zu einer weitgehenden, jedoch nicht vollständigen, Wiederherstellung der „physiologischen” Surfactant-Merkmale in der bronchoalveolären Lavageflüssigkeit (BALF) und zur Wiedereröffnung atelektatischer Lungenbezirke mit konsekutiver Reduktion des intrapulmonalen Shunt-Flusses. Darüber hinaus wurde tendenziell in der Therapiegruppe eine niedrigere Letalität beobachtet. Eine kontrollierte Studie prüft derzeit an einem größeren Patientenkollektiv mit ARDS den Einfluß einer transbronchialen Surfactant-Applikation auf die Mortalität dieses Erkrankungsbildes.
    Notes: Summary 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 of the alveolar surfactant system have since 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 (IRDS), which is known to be triggered primarily by a lack of surfactant material. Mechanisms of surfactant alterations in ARDS include: lack of surface-active compounds, changes in the relative composition of the surfactant constituents, alteration of the extracellular surfactant subtype distribution, inhibition of surfactant function by plasma protein leakage, and damage/inhibition of surfactant compounds by inflammatory mediators.¶   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. 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 application. Accordingly, acute improvement of gas exchange was encountered in two recently performed pilot studies addressing the safety and efficacy of a transbronchial application of large quantities of exogenous surfactant material. In parallel to a far reaching, but yet not complete restoration of „physiological” surfactant properties in BALF, re-opening of formerly collapsed lung regions with concomitant reduction of intrapulmonary shunt flow was noticed. Although not the primarily goal in these pilot studies, a tendency towards lower mortality in the surfactant treatment groups was noted. At present, a controlled study enrolling higher patient numbers is being performed to probe the impact of a transbronchial surfactant administration on the outcome of ARDS patients.
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  • 10
    ISSN: 1435-1420
    Keywords: Key words Acute/adult respiratory distress syndrome ; prostacyclin ; primary pulmonary hypertension ; nitric oxide ; Schlüsselwörter Acute/adult respiratory distress syndrome ; Prostazyklin ; Primäre pulmonale Hypertonie ; Stickstoffmonoxid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Trotz ihrer ausgeprägten vasodilatativen Potenz in der pulmonalen Strombahn sind die Indikationen zur intravenösen Applikation der vasodilatativen Prostanoide PGE1 und PGI2 durch fehlende pulmonale und intrapulmonale Selektivität begrenzt. Ein therapeutischer Ansatz stellt die ambulante intravenöse Dauertherapie bei Patienten mit primärer pulmonaler Hypertonie (PPH) vor (Herz-)Lungentransplantation dar. Bei Patienten mit adult respiratory distress syndrome (ARDS) führen PGE1 und PGI2 zu einer Abnahme des gesamtperipheren Widerstandes (fehlende pulmonale Selektivität), und die generelle pulmonale Vasodilatation induziert oder verstärkt Ventilations-Perfusions-Verteilungsstörungen mit begleitender Verschlechterung des Gasaustausches (fehlende intrapulmonale Selektivität). Die transbronchiale PGI2-Applikation (Aerosol) dagegen erzielt eine pulmonale und intrapulmonale Selektivität, die ein fast identisches Wirkungsprofil erreicht, wie der selektive pulmonale Vasodilatator Stickstoffmonoxid (NO). Darüber hinaus liegen erste Langzeiterfahrungen mit der repetitiven Aerosol-Applikation des länger wirkenden Iloprost bei Patienten mit schwerster pulmonaler Hypertonie vor.
    Notes: Summary The vasodilatory prostanoids PGE1 and PGI2 possess strong vasodilatory potency in the pulmonary circulation. Their application is, however, limited by the lack of pulmonary and intrapulmonary selectivity. By use of chronic ambulatory PGI2-infusion, patients with primary pulmonary hypertension (PPH) may be bridged for (heart-) lung transplantation. In patients with adult respiratory distress syndrome (ARDS), PGE1 and PGI2 lower the pulmonary vascular resistance, but may also decrease the systemic pressure (limited pulmonary selectivity) and increase ventilation-perfusion-mismatch, accompanied by an impairment of gas exchange (limited intrapulmonary selectivity). Application of PGI2 via the transbronchial route (aerosol) may achieve pulmonary and intrapulmonary selectivity with an efficacy profile comparable to that of the selective pulmonary vasodilator nitric oxide (NO). Repetitive aerosol application of the stable PGI2 analogue iloprost is under consideration for long-term treatment of patients with severe pulmonary hypertension such as primary pulmonary hypertension.
    Type of Medium: Electronic Resource
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