慢性应激抑郁大鼠模型心脏电生理变化与5-羟色胺、生长相关蛋白-43影响的研究

Serotonin Effect on Change between Cardiac Electrophysiology and Growth-Associated Protein-43 in Unpredictable Chronic Mild Stress of Depression in Mice

摘要: 目的：探讨慢性应激抑郁大鼠模型5-羟色胺(5-HT)对心脏局部组织生长相关蛋白-43(GAP-43)及动作电位的影响。方法：随机将20只大鼠分为对照组和抑郁组，对抑郁组大鼠进行连续21天的慢性应激。应用电生理仪纪录心率、心房、心室局部组织动作电位时间(APD)，对左心室心尖部行5-HT及GAP-43免疫染色。结果：抑郁组大鼠慢性应激后的糖水消耗试验、自主活动得分均明显低于对照组，差异有显著统计学意义(P < 0.01)。抑郁组大鼠心率高于对照组，差异有统计学意义(P < 0.05)。抑郁组大鼠心房、心室组织动作电位时间低于对照组大鼠，差异有统计学意义(P < 0.05)。抑郁组大鼠心室组织5-羟色胺及GAP-43递质含量高于对照组大鼠，差异有统计学意义(P < 0.01)。结论：慢性应激所致的抑郁导致交感神经平衡紊乱及5-羟色胺及GAP-43递质含量增多，明显缩短大鼠心房、心室动作电位时程，破坏了心室电生理一致性，这可能是抑郁导致心律失常的机制之一。

Abstract: Objective: To explore electrophysiologic characteristics of action potential and serotonin, growth-associated protein-43 (GAP-43) of heart location tissue in chronic stress mice. Methods: Twenty rats were randomly divided into two groups, 10 rats exposed to 21 consecutive days of unpredicted chronic mild stress as depression models, and 10 rats as normal controls. After intraperitioneal injection of choral hydrate (0.3 ml/100 mg), heart rats, atrial and ventricular local tissue field action potential duration (fAPD) were recorded by electrophysiological technology. Immunohistochemical stain, quantitative analysis of 5-HT and GAP-43 in the local heart tissue of depression group and control group were achieved by computerized image system. Results: There was significantly difference in glucose consume, total activity, heart rats between the two groups (p < 0.01, p < 0.05). The atrium and ventricular local tissue APD in depression model group were lower than that in normal group (p < 0.05). the positive index(PI) of 5-HT and GAP-43 increased in the local tissue of heart in depression model group, the PI of depression model group was much higher than in control group (p < 0.01). Conclusions: The increased heart rate, decreased fADP in atrial and ventricular tissue and increased PI of 5-HT and GAP-43 are the typical electrophysiologic characteristics of chronic depressive mice models made by unpredicted chronic mild stress method, stress depression may lead to arrhythmia through abnormal sympathetic nerve tension and serotonin change.