Abstract
Depression is generally a recurrent psychiatric disorder. Evidence shows that depression and cardiovascular diseases are common comorbid conditions, but the specific pathological mechanisms remain unclear. The purpose of this study is to determine the effects of depression induced by chronic unpredictable mild stress (CUMS) on myocardial injury and to further elucidate the biological mechanism of depression. Rats were used as a model. The CUMS procedure lasted for a total of 8 weeks. After 4 weeks of CUMS, treated rats exhibited a reduced sucrose preference and changes in scores on an open field test, body weight and content of 5-HT in the brain as compared with the values of these variables in controls. These changes indicated depression-like changes in CUMS rats and demonstrated the feasibility of the depression model. In addition, pathological changes in the myocardium and increased cardiomyocyte apoptosis demonstrated that myocardial injury had occurred after 6 weeks of CUMS and had increased significantly by the end of 8 weeks of CUMS. Plasma serotonin (5-HT), norepinephrine (NE) and epinephrine (E), all depression-related neuroendocrine factors, were measured by HPLC-ECD techniques, and the content of plasma corticosterone (GC) was evaluated by an I125–cortisol radioactivity immunoassay in control and CUMS rats. The results indicated that 5-HT had decreased, whereas NE, E and GC had increased in CUMS rats, and these factors might be associated with depression-induced myocardial injury. The effects of 5-HT, NE and GC on the survival rate of cultured cardiomyocytes were determined using an orthogonal design. The results showed that 5-HT was a more important factor affecting cell survival than GC or NE. The results suggested that normal blood levels of 5-HT had a cytoprotective effect. The neuroendocrine disorders characterized by decreased 5-HT combined with increased GC and NE mediated the occurrence of depression-induced myocardial injury.
Highlights
Cardiovascular disease (CVD) is a major cause of death in developed countries [1]
We found that chronic unpredictable mild stress caused a significant loss of body weight (Fig. 1A)
Our results showed that rats exposed to chronic unpredictable mild stress (CUMS) for 8 weeks had damaged cardiac histiocytes but that sertraline hydrochloride protected the rats from CUMS-induced myocardial injury (Fig. 4D)
Summary
Cardiovascular disease (CVD) is a major cause of death in developed countries [1]. At the beginning of the 20th century, less than 10% of world mortality was related to CVD [2]. The association between CVD and depression is well established and is suggested to be bidirectional [3]. Depressed mood has been linked to CVD risk factors in patients with and without baseline cardiac disease [4], major depression is an independent risk factor for cardiovascular mortality and morbidity [5,6]. Biological mechanisms that might link these two conditions together include the hypothalamic–pituitary–adrenal (HPA) axis, changes of arterial elasticity and endothelial function [7,8]. While the exact mechanisms linking depression and increased cardiovascular risk remain poorly understood
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