9 4 3 6 4
论文已发表
注册即可获取德孚的最新动态
IF 收录期刊
- 3.3 Breast Cancer (Dove Med Press)
- 3.4 Clin Epidemiol
- 2.5 Cancer Manag Res
- 2.9 Infect Drug Resist
- 3.5 Clin Interv Aging
- 4.7 Drug Des Dev Ther
- 2.7 Int J Chronic Obstr
- 6.6 Int J Nanomed
- 2.5 Int J Women's Health
- 2.5 Neuropsych Dis Treat
- 2.7 OncoTargets Ther
- 2.0 Patient Prefer Adher
- 2.3 Ther Clin Risk Manag
- 2.5 J Pain Res
- 2.8 Diabet Metab Synd Ob
- 2.8 Psychol Res Behav Ma
- 3.0 Nat Sci Sleep
- 1.8 Pharmgenomics Pers Med
- 2.7 Risk Manag Healthc Policy
- 4.2 J Inflamm Res
- 2.1 Int J Gen Med
- 4.2 J Hepatocell Carcinoma
- 3.7 J Asthma Allergy
- 1.9 Clin Cosmet Investig Dermatol
- 2.7 J Multidiscip Healthc
已发表论文
氟西汀对心肌梗塞后抑郁模式下大鼠活体电生理学的影响和机制
Authors Liang J, Yuan X, Shi S, Wang F, Chen Y, Qu C, Chen J, Hu D, Yang B
Published Date February 2015 Volume 2015:9 Pages 763—772
DOI http://dx.doi.org/10.2147/DDDT.S75863
Received 15 October 2014, Accepted 20 November 2014, Published 10 February 2015
Approved for publication by Professor Shu-Feng Zhou
Background: Major depression is diagnosed in 18% of patients following myocardial infarction (MI), and the antidepressant fluoxetine is shown to effectively decrease depressive symptoms and improve coronary heart disease prognosis. We observed the effect of fluoxetine on cardiac electrophysiology in vivo in a rat model of post-MI depression and the potential mechanism.
Methods and results: Eighty adult male Sprague Dawley rats (200–250 g) were randomly assigned to five groups: normal control (control group), MI (MI group), depression (depression group), post-MI depression (model group), and post-MI depression treated with intragastric administration of 10 mg/kg fluoxetine (fluoxetine group). MI was induced by left anterior descending coronary artery ligation. Depression was developed by 4-week chronic mild stress (CMS). Behavior measurement was done before and during the experiment. Electrophysiology study in vivo and Western blot analysis were carried on after 4 weeks of CMS. After 4 weeks of CMS, depression-like behaviors were observed in the MI, depression, and model groups, and chronic fluoxetine administration could significantly improve those behaviors (P <0.05 vs model group). Fluoxetine significantly increased the ventricular fibrillation threshold compared with the model group (20.20±9.32 V vs 14.67±1.85 V, P <0.05). Expression of Kv4.2 was significantly reduced by 29%±12%, 24%±6%, and 41%±15%, respectively, in the MI group, CMS group, and model group, which could be improved by fluoxetine (30%±9%). But fluoxetine showed no improvement on the MI-induced loss of Cx43.
Conclusion: The susceptibility to ventricular arrhythmias was increased in depression and post-MI depression rats, and fluoxetine may reduce the incidence of ventricular arrhythmia in post-MI depression rats and thus improve the prognosis. This may be related in part to the upregulation of Kv4.2 by fluoxetine.
Methods and results: Eighty adult male Sprague Dawley rats (200–250 g) were randomly assigned to five groups: normal control (control group), MI (MI group), depression (depression group), post-MI depression (model group), and post-MI depression treated with intragastric administration of 10 mg/kg fluoxetine (fluoxetine group). MI was induced by left anterior descending coronary artery ligation. Depression was developed by 4-week chronic mild stress (CMS). Behavior measurement was done before and during the experiment. Electrophysiology study in vivo and Western blot analysis were carried on after 4 weeks of CMS. After 4 weeks of CMS, depression-like behaviors were observed in the MI, depression, and model groups, and chronic fluoxetine administration could significantly improve those behaviors (P <0.05 vs model group). Fluoxetine significantly increased the ventricular fibrillation threshold compared with the model group (20.20±9.32 V vs 14.67±1.85 V, P <0.05). Expression of Kv4.2 was significantly reduced by 29%±12%, 24%±6%, and 41%±15%, respectively, in the MI group, CMS group, and model group, which could be improved by fluoxetine (30%±9%). But fluoxetine showed no improvement on the MI-induced loss of Cx43.
Conclusion: The susceptibility to ventricular arrhythmias was increased in depression and post-MI depression rats, and fluoxetine may reduce the incidence of ventricular arrhythmia in post-MI depression rats and thus improve the prognosis. This may be related in part to the upregulation of Kv4.2 by fluoxetine.
Keywords: depression, myocardial infarction, electrophysiology, arrhythmias, pharmacology
