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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 21 (1995), S. 1003-1008 
    ISSN: 1432-1238
    Keywords: Oleic acid ; Tranexamic acid ; Pulmonary vascular permeability ; Diphenhydramine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective Activation of fibrinolysis is implicated in the development of vascular injury in certain lung injuries. It has yet to be reported that activation of plasmin is involved in extravasation caused by oleic acid (OA). We examined whether or not plasmin is involved in pulmonary extravasation by OA. Design Prospective trial. Setting University laboratory. Subjects A total of 78 guinea pigs (498.9±10.6 g). Interventions Evans blue (EB) was administered to anesthetized guinea pigs. Subsequently four protocols were followed: (1) After 1 min, 60 μl/kg of OA was injected. Perfusion was performed 30, 60 or 90 min after OA injection to wash out intravascular EB. (2) After 1 min, 15, 30 or 60 μl/kg of OA was injected. (3) Tranexamic acid (TA) (2 g/kg) or saline was administered 30 min before OA (15 μl/kg) injection. (4) Diphenhydramine hydrochloride (2.9 mg/kg) or saline was administered 7 min before OA (15 μl/kg) injection. Measurement and results Except in protocol 1, the chest cavity was opened 90 min after OA injection. Perfusion was then performed. Airway was separated into four parts from trachea to distal bronchus. EB was extracted from the tissues and measured. OA caused an extravasation throughout airways in a time-and dose-dependent manner. Extravasation was more conspicuous in peripheral tissues. TA significantly attenuated extravasation, while diphenhydramine hydrochloride did not. Conclusions It is suggested that plasmin, but not histamine, is involved in extravasation by OA. Inhibition of plasmin can be an effective strategy for treatment of this kind of lung injury.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 24 (1998), S. 709-715 
    ISSN: 1432-1238
    Keywords: Key words Oleic acid ; fMLP ; N -acetyl-L-cysteine ; Elastase ; Superoxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Objective: Oleic acid (OA) can produce a lung injury similar to the adult respiratory distress syndrome (ARDS). Elastase and superoxides are thought to have an effect in ARDS. However, the effect that elastase and superoxide have in OA lung injury is unclear. To examine their involvement in OA lung injury, we tested the effects of methoxysuccinyl-alanyl-alanyl-prolyl-valyl chloromethyl ketone (MAAPVCK), an elastase inhibitor, and N -acetyl-L-cysteine (NAC), an active oxygen scavenger, on the increase in pulmonary vascular permeability caused by OA. We also examined whether OA stimulated elastase and/or superoxide release from polymorphonuclear leukocytes (PMNs). Design: Prospective trial. Setting: University laboratory. Interventions: (1) Guinea pigs were anesthetized. MAAPVCK (2.5 mg/kg) or NAC (150 mg/kg) was infused over OA (15 μl/kg) injection. Evans blue was used to measure vascular permeability. (2) PMNs were isolated from the blood of guinea pigs and rats. Elastase release was measured with MeO-Suc-Ala-Ala-Pro-Val-7-amino-4-methyl-coumarin. Superoxide production was measured by the ferricytochrome c reduction method. Measurements and results: OA caused pulmonary hemorrhage and an increase in vascular permeability. MAAPVCK and NAC significantly attenuated the increase in vascular permeability in distal bronchus and trachea, respectively. OA induced superoxide production from PMNs in guinea pigs, but elastase release from PMNs was not detected. Conclusions: These results suggest that elastase and superoxide are involved in OA lung injury.
    Type of Medium: Electronic Resource
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