Department of Cardiology, The Six Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, Qingyuan, China.
Department of Cardiology, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China.
Biomed Res Int. 2018 Mar 7;2018:8697913. doi: 10.1155/2018/8697913. eCollection 2018.
The aim of this study was to investigate the potential mechanisms by which chronic unpredictable mild stress (CMS) might induce cardiovascular disease.
Twenty male Sprague-Dawley rats (weighing 180-250 g) were divided into the CMS group (CMS for 3 weeks) and control group ( = 10/group). Sucrose solution consumption, sucrose solution preference rate, and the open field test (horizontal and vertical movements) were used to confirm the establishment of the CMS model. Heart rate was determined in Langendorff-perfused hearts, and field action potential duration (FAPD) was measured in cardiac atrial tissue, cardiac ventricular tissue, and thoracic spinal cord segments 1-5. The expressions of serotonin (5-HT) and growth-associated protein-43 (GAP-43) in cardiac ventricular tissue were analyzed using immunohistochemistry and immunofluorescence.
Compared with the control group, sucrose solution consumption, sucrose solution preference rate, horizontal movement, and vertical movement were significantly lower in the CMS group ( < 0.01). The CMS group exhibited significant decreases in atrial and ventricular FAPDs ( < 0.05), as well as significant increases in heart rates ( < 0.05) and T1-5 spinal cord FAPD ( < 0.01), as compared with the control group. The expressions of 5-HT and GAP-43 in cardiac ventricular tissue were significantly higher in the CMS group than in controls ( < 0.01).
CMS causes cardiac and T1-5 spinal cord electrophysiological abnormalities as well as increased cardiac expression of 5-HT and GAP-43, indicating that CMS could potentially increase the risk of cardiovascular disease.
本研究旨在探讨慢性不可预测轻度应激（CMS）诱导心血管疾病的潜在机制。
将 20 只雄性 Sprague-Dawley 大鼠（体重 180-250g）分为 CMS 组（CMS 处理 3 周）和对照组（每组 n=10）。采用蔗糖溶液消耗量、蔗糖溶液偏好率和旷场试验（水平和垂直运动）来确认 CMS 模型的建立。在 Langendorff 灌流心脏中测定心率，在心房组织、心室组织和胸段 1-5 脊髓组织中测量场动作电位时程（FAPD）。采用免疫组织化学和免疫荧光法分析心室组织中 5-羟色胺（5-HT）和生长相关蛋白-43（GAP-43）的表达。
与对照组相比，CMS 组的蔗糖溶液消耗量、蔗糖溶液偏好率、水平运动和垂直运动显著降低（ < 0.01）。与对照组相比，CMS 组的心房和心室 FAPD 显著降低（ < 0.05），心率显著升高（ < 0.05），T1-5 脊髓 FAPD 显著升高（ < 0.01）。CMS 组心室组织中 5-HT 和 GAP-43 的表达明显高于对照组（ < 0.01）。
CMS 导致心脏和 T1-5 脊髓电生理异常，以及心脏 5-HT 和 GAP-43 表达增加，表明 CMS 可能增加心血管疾病的风险。
