کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10954472 | 1097906 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Prevention of cardiac remodeling after myocardial infarction in transgenic rats deficient in brain angiotensinogen
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
intracerebroventricularACEICVTNFAT1RASChFRAASaldosterone - آلدوسترون angiotensin converting enzyme - آنزیم تبدیل آنژیوتانسینMyocardial infarction - آنفارکتوس میوکاردangiotensin - آنژیوتانسینangiotensin II type 1 - آنژیوتانسین II نوع 1Angiotensinogen - آنژیوتانسینوژنSprague–Dawley - اسپراگ داولیInfarction - انفارکتوسAng - اینCardiac remodeling - بازسازی قلبright ventricle - بطن راستleft ventricle - بطن چپTransgenic - تراریختهCNS - دستگاه عصبی مرکزیStar - ستارهSeptum - سپتومInterventricular septum - سپتوم بین دهانهRenin–angiotensin system - سیستم رنین-آنژیوتانسینrenin–angiotensin–aldosterone system - سیستم رنین-آنژیوتانسین-آلدوسترونcentral nervous system - سیستم عصبی مرکزیtumor necrosis factor - فاکتور نکروز تومورFibrosis - فیبروز یا فساد الیافBrain - مغزcongestive heart failure - نارسایی احتقانی قلبSteroidogenic acute regulatory protein - پروتئین حاکم استروئیدوژنیک حاد
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The brain renin-angiotensin-aldosterone system (RAAS) plays a major role in cardiac remodeling after myocardial infarction (MI). To assess the contribution of the brain RAAS in the activation of the cardiac RAAS post-MI, transgenic (TG) rats deficient in brain angiotensinogen and Wistar rats with intracerebroventricular (ICV) infusion of spironolactone were studied. An MI was induced by acute coronary artery ligation. TG and control Sprague-Dawley (SD) rats were followed for 8Â weeks and Wistar rats for 6Â weeks. Infarct sizes, % of left ventricle (LV) area, were in the 30-33% range. In SD rats at 8Â weeks post-MI, internal circumference, interstitial and perivascular fibrosis, cardiomyocyte diameter in the LV and right ventricle (RV), laminin and fibronectin in the LV, and lung weights were increased. Aldosterone was increased markedly in both the LV and RV at 8Â weeks post-MI. In TG rats, the MI-induced increases of RV internal circumference and weight were prevented and increases of lung weight and LV internal circumference were significantly inhibited. In TG rats, the post-MI increases of interstitial fibrosis and cardiomyocyte diameter were prevented in septum and RV and significantly inhibited in the peri-infarct zone of the LV. The increases in perivascular fibrosis, laminin and fibronectin were prevented in the LV. In TG rats, cardiac aldosterone did not increase. In Wistar rats at 6Â weeks post-MI, aldosterone was markedly increased in the LV, but not in the RV. This increase was prevented by ICV infusion of spironolactone. These findings support the pivotal role of locally produced angiotensin II in the brain in cardiac remodeling post-MI. The brain RAAS appears to activate a cascade of events, among others an increase in cardiac aldosterone, which play a major role in cardiac remodeling post-MI.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 39, Issue 3, September 2005, Pages 521-529
Journal: Journal of Molecular and Cellular Cardiology - Volume 39, Issue 3, September 2005, Pages 521-529
نویسندگان
Avtar Lal, John P. Veinot, Detlev Ganten, Frans H.H. Leenen,