کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2846665 1571303 2016 12 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Induced hypernatraemia is protective in acute lung injury
ترجمه فارسی عنوان
هیپرناترمی منجر به آسیب های حاد ریوی می شود
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی فیزیولوژی
چکیده انگلیسی


• Administration of hypertonic saline can be used to induce hypernatraemia.
• Induced hypernatraemia leads to amelioration of lung injury.
• Hypertonic saline could be used as a therapeutic option in patients with ARDS.

BackgroundSucrose induced hyperosmolarity is lung protective but the safety of administering hyperosmolar sucrose in patients is unknown. Hypertonic saline is commonly used to produce hyperosmolarity aimed at reducing intra cranial pressure in patients with intracranial pathology. Therefore we studied the protective effects of 20% saline in a lipopolysaccharide lung injury rat model. 20% saline was also compared with other commonly used fluids.MethodsFollowing lipopolysaccharide-induced acute lung injury, male Sprague Dawley rats received either 20% hypertonic saline, 0.9% saline, 4% albumin, 20% albumin, 5% glucose or 20% albumin with 5% glucose, i.v. During 2 h of non-injurious mechanical ventilation parameters of acute lung injury were assessed.ResultsHypertonic saline resulted in hypernatraemia (160 (1) mmol/l, mean (SD)) maintained through 2 h of ventilation, and in amelioration of lung oedema, myeloperoxidase, bronchoalveolar cell infiltrate, total soluble protein and inflammatory cytokines, and lung histological injury score, compared with positive control and all other fluids (p ≤ 0.001). Lung physiology was maintained (conserved PaO2, elastance), associated with preservation of alveolar surfactant (p ≤ 0.0001).ConclusionIndependent of fluid or sodium load, induced hypernatraemia is lung protective in lipopolysaccharide-induced acute lung injury.

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ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Respiratory Physiology & Neurobiology - Volume 227, 15 June 2016, Pages 56–67
نویسندگان
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