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目的:研究慢性多重应激大鼠心律失常和心房肌细胞内钙离子浓度及血清儿茶酚胺浓度变化,分析钙离子阻滞剂维拉帕米对应激性心律失常的抑制作用。方法:健康雄性SD大鼠随机分为A组(应激组)、B组(应激+维拉帕米组)和C组(对照组)。选用噪声加足底电击、强迫游泳和束缚加夜间光照的复合刺激为应激源,建立大鼠慢性多重应激模型。B组大鼠饲以钙离子阻滞剂维拉帕米。记录心电图,分析各组心律失常的类型、心律失常事件次数。测定实验前后血清儿茶酚胺含量,实验结束后,测定心房肌细胞内钙离子浓度。结果:实验结束后A、B两组大鼠全部记录到心律失常,A组大鼠出现较多类型的心律失常(窦性心律不齐、房性期前收缩、室性期前收缩、房性期前收缩和未下传、室上性心动过速、阵发性室速),B组记录到室性期前收缩(ventricular premature beats,VPB)和房性期前收缩(atrial premature beats,APB)。B组大鼠出现心律失常时间较晚(A组:17±4d;B组:25±3d,p<0.01)、心律失常发生频率低于A组(VPB:A=2.0±0.4;B=0.8±0.06,p<0.01events/min,APB:A=1.8±0.3;B=0.3±0.05events/min,p<0.01)。实验结束后,A、B两组血清去甲肾上腺素(norepinephrine,NE)和肾上腺素(epinephrine,Epi)水平增高,并高于对照组,B组低于A组(NE:A=2,617±344pg/ml;B=751±146pg/ml,P<0.01;Epi:A=1,635±224pg/ml;B=538±106pg/ml,P<0.01)。B组动物心房肌细胞内钙离子浓度较A组低(A=215±26nmol/L;B=101±15nmol/L,P<0.01)。结论:钙离子阻滞剂维拉帕米可阻止心房肌细胞钙离子内流和减少儿茶酚胺释放水平进而延缓慢性多重应激诱导的心律失常和降低其发生率。
OBJECTIVE: To study the changes of cardiac arrhythmia and atrial myocytes intracellular calcium concentration and serum catecholaminergic concentrations in chronic multiple stress rats, and to analyze the inhibitory effect of calcium antagonist verapamil on stress arrhythmias. Methods: Healthy male Sprague-Dawley rats were randomly divided into group A (stress group), group B (stress + verapamil group) and group C (control group). Select the noise plus footing shock, forced swimming and restraint plus night light compound stimuli as a stress source, the establishment of rat chronic multiple stress model. Rats in group B were given calcium antagonist verapamil. ECG recording, analysis of the types of arrhythmias in each group, the number of arrhythmic events. Determination of serum catecholamines before and after the experiment, after the end of the experiment, determination of atrial myocytes intracellular calcium concentration. Results: After the experiment, all the rats in group A and B recorded arrhythmia. A group of rats showed more types of arrhythmia (sinus arrhythmia, atrial contraction, ventricular premature ventricular contraction, atrial Systolic and non-premature ventricular contractions, supraventricular tachycardia and paroxysmal supraventricular tachycardia), group B recorded ventricular premature beats (VPB) and atrial premature beats (APB ). The incidence of arrhythmia in group B was late (group A: 17 ± 4 days; group B: 25 ± 3d, p <0.01); the frequency of arrhythmia was lower in group B than that in group A (VPB: A = 2.0 ± 0.4; ± 0.06, p <0.01events / min, APB: A = 1.8 ± 0.3; B = 0.3 ± 0.05events / min, p <0.01). At the end of the experiment, the serum levels of norepinephrine (NE) and epinephrine (Epi) in group A and group B were significantly higher than those in control group, and were lower in group B than in group A (NE: A = 2,617 ± 344pg / ml; B = 751 ± 146 pg / ml, P <0.01; Epi: A = 1, 635 ± 224 pg / ml; B = 538 ± 106 pg / ml, P <0.01). The concentration of calcium in atrial myocytes in group B was lower than that in group A (A = 215 ± 26nmol / L; B = 101 ± 15nmol / L, P <0.01). CONCLUSION: Verapamil, a calcium-ion blocker, can prevent influx of intracellular Ca2 + and decrease catecholamine release in atrial myocytes and thus delay chronic multiple stress-induced arrhythmia and decrease its incidence.