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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
    Electronic Resource
    Electronic Resource
    Springer
    Der Internist 40 (1999), S. 696-709 
    ISSN: 1432-1289
    Keywords: Schlüsselwörter Hypertonie ; pulmonale ; pulmonale Hypertonie ; Evian-Klassifikation ; pulmonale Hypertonie ; Cor pulmonale ; hypoxische pulmonale Vasokonstriktion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Zum Thema Die vorliegende Arbeit befaßt sich im Hinblick auf die pulmonale Hypertonie zunächst mit der Physiologie und den Besonderheiten der pulmonalen Strombahn, danach mit den vasokonstriktiven und vasodilatativen Mechanismen und ihrer biochemischen Regulation. Von großer Bedeutung ist dabei die hypoxische pulmonale Vasokonstriktion, die eingehend besprochen wird. Unter pathophysiologischen Gesichtspunkten führen unterschiedliche Mechanismen zur pulmonalen Hypertonie mit 3 Schweregraden. Dabei kommt der rechtsventrikulären Adaptation große prognostische Wichtigkeit zu: zunächst hypertrophiert der rechte Ventrikel, danach dilatiert er. Welche Faktoren Einfluß auf das Remodelling nehmen, ist unbekannt. Ob die Vasokonstriktion anfänglich alleiniger Auslöser der pulmonalen Hypertonie ist und/oder ob es primäre Störungen der Endothelzellen sind, wird ebenso wie die Bedeutung von Thrombosen diskutiert. Mechanischer Streß, Polyglobulie und In-situ-Thrombose bilden ein positives, Stickstoffmonoxid und ANP ein negatives Feedback. Eingehend wird abschließend die Klassifikation der verschiedenen Formen der pulmonalen Hypertonie erörtert: Die primäre und isolierte pulmonale Hypertonie sowie die sekundäre pulmonale Hypertonie, zu der die chronische alveoläre Hypoxie, interstitielle Lungenerkrankungen und die kardiogene pulmonale Hypertonie mit kongestiver Herzkrankheit, Eisenmenger-Syndrom und chronischer Lungenembolie zählen.
    Type of Medium: Electronic Resource
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