慢性应激大鼠抑郁模型心肌纤维化改变及场电位变化的研究

目的 探讨慢性应激抑郁大鼠模型的心脏局部组织的病理及场电位变化.方法 Sprague-Dawley雄性大鼠20只,体质量180～250 g,随机分为抑郁组(10只)和对照组(10只).用Cronli方法 建立慢性轻度不可预见性应激抑郁模型,并对抑郁组大鼠在慢性应激前后进行糖水消耗试验和旷场行为测试.应用微电极阵记录技术观察大鼠的心率、心房及心室肌组织局部场电位时程(fAPD)的变化规律及左心室心尖部苏木素伊红HE染色和Massion染色.结果 (1)抑郁组大鼠慢性应激后心率(107±18)次/min]显著高于对照组(99±9)次/min]、心房肌组织fAPD(83.1±4.6)ms]显著长于对照组(45.8±3.7)ms],场电位离散度(628±90)ms]大于对照组(349±69)ms];(2)抑郁组心室肌局灶性炎症细胞浸润,心肌纤维间质胶原纤维增生.结论慢性应激大鼠抑郁模型心率、心房组织fAPD及其离散度的改变,是慢性应激致大鼠心肌炎症及心肌纤维化进而增加心肌组织电兴奋的离散度,这可能慢性抑郁性心律失常的基础.

Electrophysiological study on myocardial fibrosis and heart tissue action potential in chronic stress rat model

Objective To investigate electmphysiological characteristics of the heart tissue action potential by a technique of microelectrode arrays(MEA)and pathological change in chronic stress rats.Methotis Twenty SD rats were randomly divided into depressive model group (unpredicted chronic stresses rat models made by Cronli methods.n=10)and normal control group(n=10).The rats behavior was observed with open field test and sucrose consumption test before and after stress.After intraperitoneal injection of pentobarbital anesthesia(40 mg/kg),heart rate,atrium ventricular local tissue field action potential duration(fAPD)were recorded by microelectrode arrays(MEA)technique.Cardiac tissues were stained with HE staining and Masson staining.Results There was significantly differences in-glucose consume,total activity(P＜0.01)between depressive group and control one.The heart rate incrcased from baseline(99±9)to(107±18)beals per minute,the fAPD of atrium tissue increased from baseline(45.8±3.7)ms to(83.1±4.6)ms,the fAPD dispersion(FAPD)increased from baseline(349±69)ms to(628±90 ) ms in atrium of depressive rat models.Massion stain showed the collagen of the lesion was less in normal group than that in depressive group,and HE stain showed the inflammatory cell infiltration in myocardial tissue.Conclusion The increased heart rate,prolonged fAPD of atrium tissue and increased FAPD in atrium tissue are the typical electrophysiological characteristics of cbronic depressive rat models,which may lead to arrhythmia through fibrosis and inflammatory cell infiltration in myocardial tissue.