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抑郁动物模型中心肌的结构和电重构。

Structural and electrical myocardial remodeling in a rodent model of depression.

机构信息

Department of Evolutionary and Functional Biology, University of Parma, Parma, Italy.

出版信息

Psychosom Med. 2013 Jan;75(1):42-51. doi: 10.1097/PSY.0b013e318276cb0d. Epub 2012 Dec 20.

DOI:10.1097/PSY.0b013e318276cb0d
PMID:23257930
Abstract

OBJECTIVE

Despite a well-documented association between stress and depression with cardiac morbidity and mortality, there is no satisfactory explanation for the mechanisms linking affective and cardiac disorders. This study investigated cardiac electrophysiological properties in an animal model of depression.

METHODS

Depression-relevant physiological and behavioral parameters were measured in adult male wild-type rats during and after a period of intermittent social defeat stress (n = 12) or empty cage exposure (control, n = 11). Nine days after the last defeat/empty cage exposure, high-definition epicardial mapping was performed under anesthesia.

RESULTS

Stressed animals versus controls displayed a larger reduction in the circadian amplitude of heart rate (-32% [3%] versus -13 [2%]; p = .001) and body temperature (-33% [4%] versus -5% [2%]; p = .001) rhythms, had smaller body weight gain (+11% [1%] versus +17% [1%]; p < .001), and showed a larger reduction in sucrose solution intake (-19% [6%] versus -7% [4%]; p = .006). Epicardial mapping analysis revealed a decrease in the transversal conduction velocity of the wavefront (0.23 [0.0] versus 0.27 [0.1] m/s; p = .02) and a shortening of the effective refractory period (86.8 [2.1] versus 95.9 [3.0] milliseconds; p = .01) in stressed animals. Upon killing, moderate left ventricular fibrosis was observed in the stressed group.

CONCLUSIONS

Intermittent social stress procedure is associated with depression-like symptoms and altered myocardial electrical stability in a potentially proarrhythmic manner. In particular, reduced myocardial refractoriness and impaired conduction, which are considered major determinants of arrhythmogenesis, represent possible mechanisms underlying cardiac vulnerability.

摘要

目的

尽管压力和抑郁与心脏发病率和死亡率之间存在明确的关联,但对于将情感和心脏疾病联系起来的机制还没有令人满意的解释。本研究在抑郁动物模型中研究了心脏电生理特性。

方法

在间歇社交挫败应激(n = 12)或空笼暴露(对照,n = 11)期间和之后,测量成年雄性野生型大鼠的抑郁相关生理和行为参数。在最后一次挫败/空笼暴露后 9 天,在麻醉下进行高清心外膜映射。

结果

与对照组相比,应激动物显示出更大的心率(-32%[3%]与-13[2%];p =.001)和体温(-33%[4%]与-5%[2%];p =.001)昼夜节律振幅降低,体重增加减少(+11%[1%]与+17%[1%];p <.001),蔗糖溶液摄入减少(-19%[6%]与-7%[4%];p =.006)。心外膜映射分析显示,波前的横向传导速度降低(0.23[0.0]与 0.27[0.1]m/s;p =.02),有效不应期缩短(86.8[2.1]与 95.9[3.0]毫秒;p =.01)在应激动物中。在处死时,应激组观察到中度左心室纤维化。

结论

间歇性社交应激程序与抑郁样症状和心肌电稳定性改变有关,可能具有潜在的致心律失常作用。特别是,降低的心肌不应期和受损的传导,被认为是心律失常发生的主要决定因素,代表了心脏脆弱性的可能机制。

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