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较大剂量（５００／，腹腔注射）ＣＳ２急性毒性实验大鼠心电图主要表现为ＰＲ间期、ＱＴ间期延长，Ｐ波、Ｒ波及Ｔ波电压增大及心率减慢等。结果提示ＣＳ２导致房室传导阻滞、急性心肌缺血的急性心血管毒作用以及心肌收缩力增强的“正力性效应”表现；ＣＳ２亚慢性毒性实验（染毒剂量为１６０～３２０／，每周６天，连续７周）大鼠心电图主要显示心率减慢，ＱＲＳ时限、ＰＲ间期、ＱＴ间期均延长，而Ｔ波电压下降；血压未见明显异常。提示了ＣＳ２可致心肌缺血、心室内及房室间房室传导阻滞等毒性损害作用。分析认为：ＣＳ２的心血管毒性可表现为心率减慢、急慢性心肌缺血及心脏电生理（兴奋传导）异常等。
The larger the dose (500 /, intraperitoneal injection) CS2 acute toxicity in rats ECG mainly P R interval, Q T interval prolongation, P wave, R wave and T wave voltage increases and heart rate slowed. The results suggest that CS2 results in a “positive effect” of atrioventricular block, acute cardiotoxicity of acute myocardial ischemia and myocardial contractility; CS2 subchronic toxicity test (dose of 160 ~ 320 /, each Week 6 days, 7 consecutive weeks) ECG mainly showed slow heart rate, QRS duration, P R interval, Q T interval were prolonged, while the T wave voltage drop; no significant abnormal blood pressure. Prompted CS2 can cause myocardial ischemia, intraventricular and atrioventricular block and other toxic damage. Analysis suggests that: CS2 cardiovascular toxicity can be manifested as slow heart rate, acute and chronic myocardial ischemia and cardiac electrophysiology (excited conduction) abnormalities.