کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10954739 | 1097918 | 2005 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Administration of a CO-releasing molecule induces late preconditioning against myocardial infarction
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Administration of a CO-releasing molecule induces late preconditioning against myocardial infarction Administration of a CO-releasing molecule induces late preconditioning against myocardial infarction](/preview/png/10954739.png)
چکیده انگلیسی
Mounting evidence suggests that carbon monoxide (CO) exerts powerful cytoprotective actions. CO-releasing molecules (CORMs) offer an effective means of delivering CO to tissues in vivo. The goal of the present study was to determine whether a water-soluble CORM, tricarbonylchloro(glycinato)ruthenium(II) (CORM-3), induces delayed protection against myocardial infarction 24 h later and to explore the duration of this protection. Mice received a 60-min i.v. infusion of CORM-3 or inactive CORM-3 (which does not release CO) and then, 24, 72, or 120 h later, underwent a 30-min coronary occlusion followed by 24 h of reperfusion. Pretreatment with CORM-3 24 h prior to coronary occlusion markedly reduced infarct size (24.8% ± 2.9% of the risk region vs. 43.8% ± 4.4% with inactive CORM-3). The infarct-sparing effect of CORM-3 was still evident 72 h after administration of the CO donor (20.4% ± 3.7% of the risk region vs. 41.9% ± 2.5% with inactive CORM-3) but was no longer apparent at 120 h. Both at 24 and 72 h, the protective effects of CORM-3 were equivalent to those afforded by the late phase of ischemic preconditioning (PC; 27.0% ± 2.9% and 30.3% ± 3.9% of the risk region, respectively). We conclude that the novel CO-releasing compound, CORM-3, induces delayed protection against myocardial infarction which is similar to that afforded by the late phase of ischemic PC, and that this salubrious effect is sustained for 72 h. To our knowledge, this is the first report that exposure to CO causes the heart to shift to a preconditioned phenotype. In addition, this study provides the first evidence that the cardioprotective actions of ischemic PC persist for 72 h in the mouse.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 38, Issue 1, January 2005, Pages 127-134
Journal: Journal of Molecular and Cellular Cardiology - Volume 38, Issue 1, January 2005, Pages 127-134
نویسندگان
Adam B. Stein, Yiru Guo, Wei Tan, Wen-Jian Wu, Xiaoping Zhu, Qianhong Li, Cheng Luo, Buddhadeb Dawn, Tony R. Johnson, Roberto Motterlini, Roberto Bolli,