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与大鼠心脏其他区域相比,链脲佐菌素诱导的糖尿病对窦房结动作电位的影响。

Effects of streptozotocin-induced diabetes on action potentials in the sinoatrial node compared with other regions of the rat heart.

作者信息

Howarth F C, Al-Sharhan R, Al-Hammadi A, Qureshi M A

机构信息

Department of Physiology, Faculty of Medicine & Health Sciences, United Arab Emirates University, Al Ain, Abu Dhabi, United Arab Emirates.

出版信息

Mol Cell Biochem. 2007 Jun;300(1-2):39-46. doi: 10.1007/s11010-006-9366-5. Epub 2006 Nov 25.

Abstract

In vivo biotelemetry studies have demonstrated that heart rate (HR) is progressively and rapidly reduced after administration of streptozotocin (STZ) and that the reduction in HR can be partially normalized with insulin replacement. Reductions in HR have also been reported in isolated perfused heart and superfused right atrial preparations suggesting that intrinsic defects in the heart are at least partly responsible for the bradycardia. The regional effects of STZ-induced diabetes mellitus (DM) on action potentials (APs) in the sinoatrial node (SAN), right and left atria and ventricles have been compared in the spontaneously beating Langendorff perfused rat heart 10-12 weeks after treatment. HR was significantly reduced in STZ-induced diabetic rat heart (174 +/- 9 BPM) compared to controls (241 +/- 12 BPM). The duration of AP repolarization at 50% and 70% from peak AP was significantly prolonged in SAN, right atrium and right ventricle from STZ-induced diabetic rat compared to age-matched controls. In the SAN AP duration (APD) at 50% and 70% were 51.7 +/- 2.2 and 59.5 +/- 2.3 ms in diabetic rat heart compared to 45.2 +/- 1.7 and 50.0 +/- 1.6 ms in controls, respectively. In contrast APD at 50% and 70% were not significantly altered in the left atrium and left ventricle. Regional defects in the expression and/or electrophysiology of SAN ion channels, and in particular those involved in AP repolarization, might underlie heart rhythm disturbances in the STZ-induced DM rat.

摘要

体内生物遥测研究表明,注射链脲佐菌素(STZ)后心率(HR)会逐渐且迅速降低,而补充胰岛素可使心率降低部分恢复正常。在离体灌注心脏和灌流右心房标本中也有心率降低的报道,提示心脏的内在缺陷至少部分导致了心动过缓。在治疗后10 - 12周的自发搏动Langendorff灌注大鼠心脏中,比较了STZ诱导的糖尿病(DM)对窦房结(SAN)、左右心房和心室动作电位(AP)的区域影响。与对照组(241±12次/分钟)相比,STZ诱导的糖尿病大鼠心脏的HR显著降低(174±9次/分钟)。与年龄匹配的对照组相比,STZ诱导的糖尿病大鼠的SAN、右心房和右心室在动作电位峰值的50%和70%处的复极持续时间显著延长。在糖尿病大鼠心脏的SAN中,动作电位持续时间(APD)在50%和70%处分别为51.7±2.2和59.5±2.3毫秒,而对照组分别为45.2±1.7和50.0±1.6毫秒。相比之下,左心房和左心室在50%和70%处的APD没有显著改变。SAN离子通道表达和/或电生理学的区域缺陷,特别是那些参与动作电位复极的缺陷,可能是STZ诱导的糖尿病大鼠心律失常的基础。

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