کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5960448 | 1175822 | 2015 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cardiac late Na+ current: Proarrhythmic effects, roles in long QT syndromes, and pathological relationship to CaMKII and oxidative stress
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کلمات کلیدی
PI3KICa-LIncXLQTRepolarization reserveATX-IILQT3IKrEADQTcAPDNCXDADIKSTTXCaMKIICa2+/calmodulin-dependent protein kinase II - Ca2 + / calmodulin وابسته پروتئین کیناز IIINa - INALong QT - QT طولانیROS - ROS[Ca2+]i - [Ca2 +] i[Na+]i - [Na +] Ilate sodium current - اواخر سدیم جریانearly afterdepolarization - اوایل پس از دپولیزاسیونReentry - بازگرداندنslowly activating delayed rectifier potassium current - به آرامی فعال شدن جریان پتاسیم یکسو کننده تاخیرVentricular tachycardia - تاکی کاردی بطنیtetrodotoxin - تترو دوتوکسین Corrected QT - تصحیح QTsodium current - جریان سدیمrapidly activating delayed rectifier potassium current - جریان سریع پتاسیم یکسو کننده تاخیر سریعا فعال می شودL-type calcium current - جریان کلسیم L نوعantiarrhythmic drug - داروهای ضد آرتریتranolazine - رانولازینLong QT syndrome - سندرم QT طولانیIntracellular sodium concentration - غلظت سدیم داخل سلولیintracellular calcium concentration - غلظت کلسیم داخل سلولیphosphoinositide 3-kinase - فسفینوزیتید 3-کینازtriggered activity - فعالیت را باعث می شودAction potential duration - مدت زمان بالقوه عملaction potential - پتانسیل عمل Dispersion of repolarization - پراکندگی repolarizationdelayed afterdepolarization - پس از depolarization به تعویق افتادReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
کاردیولوژی و پزشکی قلب و عروق
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Cardiac late Na+ current: Proarrhythmic effects, roles in long QT syndromes, and pathological relationship to CaMKII and oxidative stress Cardiac late Na+ current: Proarrhythmic effects, roles in long QT syndromes, and pathological relationship to CaMKII and oxidative stress](/preview/png/5960448.png)
چکیده انگلیسی
Myocyte sodium channel current that persists throughout the plateau of the cardiac action potential is referred to as late sodium current (INa-L). The magnitude of INa-L is normally small, but can increase significantly in common acute and chronic pathological settings as a result of inherited and/or acquired Na+ channelopathies that alter channel opening and closing (ie, gating), location (trafficking), or anchoring and interactions with cytoskeletal proteins. An increase in INa-L reduces repolarization reserve in atrial and ventricular myocytes and prolongs the action potential duration and the QT interval. An enhanced INa-L is a cause of long QT syndrome 3. INa-L may be a cause of afterdepolarizations, triggered arrhythmias, and spontaneous diastolic depolarization-induced automaticity. In addition, enhancement of INa-L increases both the temporal and the spatial dispersion of repolarization in the myocardium and may lead to spatially discordant action potential duration alternans, wavebreak, and reentrant arrhythmias. Positive feedback loops between increases in INa-L and the activity of Ca2+/calmodulin-dependent protein kinase II appear to contribute to the genesis of arrhythmias and to certain abnormalities of the ischemic heart. In this review, we discuss some of the more relevant experimental results, clinical findings, and insights from cellular and animal models that highlight the role of INa-L in the genesis of arrhythmias, long QT syndromes, and intracellular Ca2+ homeostasis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Heart Rhythm - Volume 12, Issue 2, February 2015, Pages 440-448
Journal: Heart Rhythm - Volume 12, Issue 2, February 2015, Pages 440-448
نویسندگان
Luiz Belardinelli, Wayne R. PhD, Sridharan PhD, Hrayr S. PhD, FHRS, John C. PhD,