Suicidality and Suicide Attempt in a Young Female on Long-Term Sertraline Treatment

Santra, Ranjita; Chaudhuri, Patralekha Ray; Dhali, Dibyendu; Mondal, Shirsendu

doi:10.4103/0253-7176.108230

Cited by 3 publications

(3 citation statements)

References 7 publications

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“…Similarly, there are some studies that indicated SRT-induced tachycardia. [45][46][47][48][49][50][51] ECG is routinely used in the determination of cardiotoxicity induced by various agents. 1 An ECG is a recording of the heart's electrical activity as a graph consisting of PQRST complexes.…”

Section: Discussionmentioning

confidence: 99%

Evidence for cardiotoxicity associated with sertraline in rats

et al. 2018

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Section: Discussionmentioning

confidence: 99%

Evidence for cardiotoxicity associated with sertraline in rats

et al. 2018

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“…The mechanism of sertraline treatment for both disorders may include direct and indirect effects. Vasodilatory, antiplatelet and endothelium- protective effects of sertraline [62] , [63] may contribute to the direct effect. The indirect effect may result from the use of sertraline to treat depression, and recovery from depression might contribute to an amelioration of heart injury.…”

Section: Discussionmentioning

confidence: 99%

A Neuroendocrine Mechanism of Co-Morbidity of Depression-Like Behavior and Myocardial Injury in Rats

Wang

Liu²,

Wu³

et al. 2014

PLoS ONE

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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.

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“…The accurate mechanism of protective function of sertraline in cardiomyocytes has not been yet clearly known. But, several studies have described that sertraline has vasodilatory role, the antiplatelet effects and protective effects of vascular endothelial cells and with the help of these factors involves in the inhibition of myocardial damage (28,29). Since, in this study we encountered a significant reduction in homocysteine and cTnI in rats in dose of 80 mg, hence, sertraline can play fundamental role in the heart protecting.…”

Section: Pharm Biomed Res 2017; 3(3): 20mentioning

confidence: 55%

Sertraline alters level of adenosine deaminase activity, oxidative stress markers and cardiac biomarkers (homocysteine cardiac troponin I) in rats

2017

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The aim of this study is whether oxidative stress markers, homocysteine (Hcy), cardiac troponin I (cTnI) and the activity of adenosine deaminase (ADA) alter following administration of different doses of sertraline. Sixty male Wistar rats were assigned into four groups. Sertraline at doses of 20, 40 and 80 mg / kg / day) were administered to three groups through gastric gavage for 90 days. The fourth group was received only distilled water. After 90 days of sertaline administration, the levels of oxidative stress biomarkers in plasma were measured. The results revealed remarkable elevation in malondialdehyde (MDA) and considerable reduction in Hcy, cTnI, antioxidant enzymes levels as superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase and paraoxonase (PON)and ADA activity in the rats that were receive sertraline at dose of 80 mg /Kg /day. The results denoted that sertraline administration at the dose of 80 mg/kg/day reduce cardiovascular biomarkers. Meanwhile, decrease of ADA activity may suggest reduction of immune function due to sertraline administration.

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Suicidality and Suicide Attempt in a Young Female on Long-Term Sertraline Treatment

Cited by 3 publications

References 7 publications

Evidence for cardiotoxicity associated with sertraline in rats

Evidence for cardiotoxicity associated with sertraline in rats

A Neuroendocrine Mechanism of Co-Morbidity of Depression-Like Behavior and Myocardial Injury in Rats

Sertraline alters level of adenosine deaminase activity, oxidative stress markers and cardiac biomarkers (homocysteine cardiac troponin I) in rats

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