高脂饮食诱导肥胖大鼠心肌细胞内钙调节机制的研究  

Experimental study on regulatory mechanism of intracellular calcium in myocardial cell of obesity prone rats induced by high-fat diet

作　　者：郝艳坤[1] 王莹[1] 孙健[1] 杨宝峰[2] 

机构地区：[1]牡丹江医学院动物技能教研室,黑龙江牡丹江157011 [2]哈尔滨医科大学药理学教研室,黑龙江哈尔滨150081

出　　处：《哈尔滨医科大学学报》2009年第4期354-356,共3页Journal of Harbin Medical University

基　　金：黑龙江省卫生厅科研课题(2007-011)

摘　　要：目的建立高脂饮食诱导肥胖易感(OP)大鼠,研究肥胖大鼠心肌细胞内钙调节的机制。方法高脂饲料喂饲健康雄性SD大鼠10周后,筛选出肥胖易感(OP)大鼠动物模型。实验结束后,处死动物,测量体脂肪含量,并收集血清,以检测血脂水平。采用酶法分离心肌细胞,Fluo-3/AM负载后采用激光共聚焦扫描显微镜观察心肌[Ca2+]i对KCl除极及咖啡因诱导的反性。结果OP大鼠肾周脂肪、睾周脂肪、网膜脂肪、体脂肪含量均显著高于基础组大鼠,甘油三酯水平和总胆固醇显著高于基础对照组。肥胖模型组心室肌[Ca2+]i的升高幅度、速度以及不同时间点的恢复程度均显著低于基础组(P<0.05)。结论肥胖心肌细胞[Ca2+]i在KCl除极后升高速度、幅度及恢复程度都发生改变,可能是肥胖心律失常发生机制之一。Objective To study the regulatory mechanism of intracellular calcium in myocardial cell of obesity prone rats induced by high-fat diet. Methods Male Sprague-Dawley（SD） rats were sieved to obesity prone（ OP）rats after fed with high fat diet for 10 weeks. After the rats were sacrificed , body fat content was measured and serum was collected to measure blood sugar and serum lipids. Myocardial cells were then isolated with Langendorff perfusion technique and [ Ca^2＋] i was measured with calcium indicator Fluo-3/AM and Laser Scanning Confocal Microscope after KC1 depolarization and caffeine-induced. Results. Inguinal fat, perirenal fat, omental fat and body fat content as well as the level of triglyeeride （TG） and total cholesterol （T-CHO）were significantly higher in OP rats than those in control group rats. The ascendant velocity, the extent of cytosolic [ Ca^2＋ ] i elevation and the restoration in OP rats group were singificantly lower compared with control group （P 〈 0. 05 ）. Conclusion The ascendant velocity, the extent of cytosolic [ Ca^2＋ ] i elevation and restoration in OP rats changed singificantly after KC1 depolarization that may be one of the mechanisms of arrhythmia in obesity prone rats.

关 键 词：肥胖 体脂肪含量 激光共聚焦扫描显微镜 细胞内钙 

分 类 号：R331.31[医药卫生—人体生理学] R-332[医药卫生—基础医学]