کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5828434 1558963 2013 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
High dose remifentanil increases myocardial oxidative stress and compromises remifentanil infarct-sparing effects in rats
ترجمه فارسی عنوان
دوز بالا رمی فنتانیل استرس اکسیداتیو قلب را افزایش می دهد و اثرات مضر انفارکتومی رمی فنتانیل را در موش صحرایی
کلمات کلیدی
رمی فنتانیل، استرس اکسیداتیو، استرس نیتروژنیک، اپیوئیدها، حفاظت قلب،
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب سلولی و مولکولی
چکیده انگلیسی
Chronic administration of high dose opioids such as morphine is known to create intracellular oxidative stress via an opioid receptor dependent mechanism and this can interfere with cellular function. This study aimed at examining whether such changes can occur following short term exposure to high concentration of remifentanil, a potent short acting opioid. We conducted a experimental study using rat myocardium and systematically quantified tissue levels of superoxide anions, malondialdehyde (MDA) and nitrotyrosine following exposure to increasing duration (15 min, 1 or 2 h) or escalating doses of remifentanil (1 μg, 5 μg, 10 μg or 20 μg/kg/min). Concurrently the susceptibility of the heart to ischaemia reperfusion injury was assessed under the similar conditions. For any given duration of remifentanil infusion, there was increasing superoxide anions generated as the dose of remifentanil was increased. MDA concentrations were significantly increased when the animal was exposed to 10 μg/kg/min for 2 h or 20 μg/kg/min for any duration. There was a trend towards an increased nitrotyrosine concentration with increasing dose of remifentanil, becoming significant when the dose was 20 μg/kg/min. The infarct limiting ability of remifentanil was compromised when the dihydroethidium fluorescence positive cell percentage exceeded 50%, MDA concentration greater than 2 nmol/mg of protein and nitrotyrosine content exceeding 1.5 μg/mg of protein. Short term high dose opioid exposure can induce oxidative changes seen previously only with chronic opioid use and this high oxidative stress environment corrupts the heart's sensitivity to be preconditioned by opioids.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: European Journal of Pharmacology - Volume 718, Issues 1–3, 15 October 2013, Pages 484-492
نویسندگان
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