کد مقاله کد نشریه سال انتشار مقاله انگلیسی ترجمه فارسی نسخه تمام متن
2192898 1098003 2017 9 صفحه PDF ندارد دانلود رایگان
عنوان انگلیسی مقاله
Norepinephrine-induced Sustained Myocardial Adaptation to Ischemia is Dependent onα1-Adrenoceptors and Protein Synthesis ☆
ترجمه فارسی عنوان
انطباق قلبی پایدار ناشی از نوراپی نفرین برای ایسکمی وابسته به onα1-آدرنرژیک و سنتز پروتئین دارد
کلمات کلیدی
نوراپی نفرین؛ سیکلوهگزیمید؛ α1 آدرنرژیک؛ ایسکمی و خونرسانی مجدد؛ انقباض میوکارد؛ موش
Norepinephrine; Cycloheximide; α1-Adrenoceptors; Ischemia and reperfusion; Myocardial contractility; Rat
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
چکیده انگلیسی

The authors have shown that stimulation of cardiacα1-adrenoceptors confers immediate cardioprotection in the isolated rat heart against post-ischemic dysfunction, and have recently demonstrated thatin vivotreatment of rats with norepinephrine (NE) induces cardiac heat shock protein 72 and myocardial adaptation to ischemia 24 h after treatment. To characterize the delayed myocardial adaptive response induced by NE further, the present study examined its time course and effects of adrenoceptor antagonism and protein synthesis inhibition on this adaptive response during optimal myocardial protection. Rats were treated with NE (3.1μmol/kg, i.p.) or normal saline (0.4 ml, i.p.), and hearts isolated at 2, 4, 24, 72 and 168 h after injection. Isolated hearts were subjected to 25 min of normothermic global ischemia and 40 min of reperfusion by the Langendorff technique, and left ventricular developed pressure (LVDP) was assessed. There was no difference in baseline LVDP among groups. Post-ischemic LVDP recovered to 44.7±2.1 mmHg in pooled saline control. LVDP was significantly improved in hearts isolated at 4, 24 and 72 h after injection of NE (66.3±3.8, 68.6±2.7 and 72.6±8.3 mmHg, respectively,P<0.05vcontrol) but not in hearts isolated at 2 or 168 h. Effects of antecedent adrenoceptor antagonism and protein synthesis inhibition were examined in hearts isolated at 72 h after NE treatment. Prazosin pretreatment (2.4μmol/kg, i.p.) abolished the delayed myocardial adaptive response induced by NE at 72 h (post-ischemic LVDP 48.3±6.1 mmHg,P>0.05vcontrol) while propranolol pretreatment (3.4μmol/kg, i.p.) had no effect (post-ischemic LVDP 67.3±3.7 mmHg,P<0.05vcontrol). Cycloheximide pretreatment (3.6μmol/kg, i.p.) also abolished the beneficial effect of NE at 72 h (post-ischemic LVDP 50.2±6.0 mmHg,P>0.05vcontrol). In conclusion, administration of NE to rats can induce delayed and sustained cardioprotection against post-ischemic myocardial dysfunction. NE-induced myocardial adaptation to ischemia at 72 h is mediated byα1-adrenoceptors and appears to require protein synthesis.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 28, Issue 9, September 1996, Pages 2017–2025
نویسندگان
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