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正常血压大鼠心肌梗死后的急性心律失常发生机制:高盐摄入的影响。

Acute arrhythmogenesis after myocardial infarction in normotensive rats: influence of high salt intake.

机构信息

Department of Physiological Sciences, Federal University of Espírito Santo, 29042-755 Vitória, ES, Brazil.

出版信息

Food Chem Toxicol. 2012 Mar;50(3-4):473-7. doi: 10.1016/j.fct.2011.11.033. Epub 2011 Nov 27.

Abstract

A high salt diet is a known risk factor for cardiovascular diseases that leads to cardiac hypertrophy and creates a substrate for arrhythmias and sudden death. However, acute arrhythmogenesis after infarction has not been studied. Male Wistar rats (21 days) received drinking water (MI) or 1% NaCl solution (MI-Salt-C) for 4 weeks. Water was given to another group for 4 weeks, and on the day before surgery, animals received a 1% NaCl solution (MI-Salt-A). Non-invasive systolic blood pressure (SBP) was obtained before surgery. Myocardial infarction (MI) was produced by permanent occlusion of the left coronary artery. Electrocardiogram was monitored during the first 30 min post-occlusion to evaluate arrhythmias. Although SBP was not altered by salt intake (SHAM: 114±2, MI: 112±2, MI-Salt-C: 115±2, MI-Salt-A: 116±4 mm Hg), ventricular hypertrophy was observed in the animals receiving chronic salt diet (SHAM: 0.22±0.008, MI: 0.23±0.007, MI-Salt-C: 0.28±0.01; MI-Salt-A: 0.23±0.01 g/cm; P<0.05). Ventricular premature beats increased in both salt-loaded groups compared to MI group (MI: 805±81, MI-Salt-C: 1145±98; MI-Salt-A: 1023±77; P<0.05). Atrioventricular blockade was only observed in animals subjected to high salt intake (MI-Salt-C: 38.9%; MI-Salt-A: 42.1%). High salt intake was associated with increased post-infarct arrhythmias; however, this effect was unrelated to ventricular hypertrophy.

摘要

高盐饮食是心血管疾病的已知危险因素,可导致心肌肥大,并为心律失常和心脏性猝死创造基础。然而,尚未研究梗死后的急性心律失常发生机制。雄性 Wistar 大鼠(21 天)在 4 周内饮用饮用水(MI)或 1%NaCl 溶液(MI-Salt-C)。另一组在 4 周内给予水,并且在手术前一天,动物接受 1%NaCl 溶液(MI-Salt-A)。手术前获得非侵入性收缩压(SBP)。通过左冠状动脉永久闭塞产生心肌梗死(MI)。在闭塞后 30 分钟内监测心电图以评估心律失常。尽管盐摄入量并未改变 SBP(SHAM:114±2,MI:112±2,MI-Salt-C:115±2,MI-Salt-A:116±4mmHg),但接受慢性盐饮食的动物出现心室肥厚(SHAM:0.22±0.008,MI:0.23±0.007,MI-Salt-C:0.28±0.01; MI-Salt-A:0.23±0.01g/cm;P<0.05)。与 MI 组相比,两种盐负荷组的室性早搏均增加(MI:805±81,MI-Salt-C:1145±98; MI-Salt-A:1023±77; P<0.05)。仅在接受高盐摄入的动物中观察到房室传导阻滞(MI-Salt-C:38.9%; MI-Salt-A:42.1%)。高盐摄入与梗死后心律失常增加有关;然而,这种作用与心室肥厚无关。

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