不同剂量异丙肾上腺素致大鼠急性心肌损伤模型的制备及评价

Preparation and evaluation of an acute myocardial injury model induced by different doses of isoproterenol in rats

目的研究不同剂量异丙肾上腺素对大鼠心功能和病理形态损伤的影响。方法SD大鼠随机分为四组,即Control组,低剂量模型组(25 mg/kg),中剂量模型组(50 mg/kg),高剂量模型组(100 mg/kg)。模型组颈部多点皮下注射不同剂量异丙肾上腺素连续2 d,Control组注射等量生理盐水。最后一次给药24 h后描计心电图(ECG)检测QRS间期,P波时程与波幅;TTC染色检测心肌梗死面积,HE染色观察心肌组织病理形态。结果与正常对照组比较,不同剂量模型组大鼠心重及左室重均明显升高(P<0.01);ECG显示,高剂量模型组P波时程增加(P<0.01),低剂量模型组与高剂量模型组P波波幅增加(P<0.05,P<0.01),同时有心律不齐的心电图表现。TTC染色和HE染色均有心肌损伤的病理改变。结论模型组大鼠心肌组织均有不同程度损伤,高剂量模型组心肌损伤最严重,为缺血/梗死类心脏疾病的动物模型制备和相关机制研究提供依据。

Objective To study the effects of different doses of isoproterenol(ISO)on cardiac function and pathological morphology in rats.Methods Sprague-Dawley rats were randomly divided into Control,low-dose model(ISO 25 mg/kg),medium-dose model(ISO 50 mg/kg),and high-dose model(ISO 100 mg/kg)groups.In the model group,different doses of ISO were injected subcutaneously at multiple points in the neck for two consecutive days whereas the Control group received the same volume of saline.Changes in heart rate,QRS interval,duration and amplitude of P-waves were detected by electrocardiogram(ECG).The myocardial infarct size was detected by TTC staining and the pathological morphology of myocardial tissues was observed by HE staining 24 hours after the last administration.Results Compared with the Control group,the heart and left ventricular weights of rats in different dose model groups were significantly increased(P<0.01)and the ECG of rats showed that the P-wave duration in the high-dose model group was increased(P<0.01),the P-wave amplitude in the low-dose and high-dose model groups was increased(P<0.05,P<0.01,respectively)and arrhythmia was present.TTC staining and HE staining showed pathological changes related to myocardial injury.Conclusions Different degrees of damage were observed in myocardial tissues of the model groups and the most serious myocardial injury was observed in the high-dose model group.This study provides a basis for animal model development and research of the mechanisms of ischemic/infarct heart disease.