阿霉素对兔心肌损伤与心肌ATP酶活性和NOS表达的关系  被引量:1

The relationship between injury of cardiac muscular tissue caused by adriamycin and the activity of adenosine triphosphatase and expression of nitric oxide synthase in rabbits

在线阅读下载全文

作  者:陈河[1] 黄先玫[2] 赵文华[1] 亢晓冬[1] 

机构地区:[1]杭州师范学院医学院组织胚胎学教研究室,浙江杭州310012 [2]浙江大学医学院附属儿童医院,杭州310012

出  处:《杭州医学高等专科学校学报》2002年第1期4-6,共3页Journal of Hangzhou Medical College

摘  要:目的 探讨阿霉素对心肌损伤与心肌ATP酶活性和NOS表达变化的关系。方法 用治疗剂量阿霉素静脉注射 ,建立兔阿霉素心肌损伤模型作为模型组 ,静脉注射生理盐水作为对照组。取心肌组织进行HE染色及超薄切片染色 ;采用Padykula及Herman法和NADPH -d酶组织化学染色 ;进行图象分析 ,数据进行统计学检验 ;观察和比较两组动物心肌组织中ATP酶和NOS的变化。结果 病理学检查和电镜观察表明模型组心肌组织和超微结构受损伤 ;酶组织化学染色和图象分析显示Ca2 + -ATP酶活性下降 ,而NOS表达上调 ,模型组与对照组相比 ,P <0 .0 1,具有显著性差异。结论 治疗剂量阿霉素能够降低心肌组织中Ca2 + -ATP酶的活性和上调NOS的表达 ,并可能是导致心肌损伤的重要原因。Objective To explore the relationship of cardiac muscular tissue injury caused by adriamycin and changes of ATPase activity and expression of NOS in rabbits.Method 9 rabbits were injected with the therapeutic dosage of Adr by vein as the cardiac muscle injury model group, 9 rabbits were injected with physiological salt solution through vein as the control group.Cardiac tissues were collected from both groups, and HE staining and ultrathin sectioning and enzyme histochemical staining were taken and image analysis were performed. Changes of the activity of ATPase and expression of NOS of the cardiac muscular tissue from two groups were observed and compared with each other through statistical analysis.Result Pathological examination and electron microscopy observation demonstrated that the cardiac muscular tissue and ultrastructures were harmed, and Ca 2+ -ATPase activity descended and expression of NOS elevated in the model group, compared with the control group, P<0.01, there were prominent difference between these two groups.Conclusion The therapeutic dosage of Adr can descend Ca 2+ -ATPase activity and elevate expression of NOS, which may be the important cause leading to cardiac muscular tissue injury.

关 键 词:阿霉素 心肌损伤 三磷酸腺苷酶 一氧化氮合酶 

分 类 号:R972[医药卫生—药品]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象