阿霉素对兔心肾损伤与一氧化氮合酶表达

目的:探讨阿霉素(Adr)对心和肾损伤与一氧化氮合酶(NOS)表达。方法:用治疗剂量阿霉素静脉注射法建立兔心、肾损伤模型组,测定兔心输出量(CO)、左心室收缩压(LVSP)、左心室舒张末压(LVEDP):取心和肾组织进行HE染色及超薄切片染色;NADPH组化染色并进行图像分析,观察动物心和肾组织中ALP、Ca~(2+)-ATP酶和 NOS的变化。结果:实验组CO、LVSP均明显低于对照组,LVEDP明显高于对照组;实验组心和肾组织的超微结构受损伤,Ca~(2+)-ATP酶活性明显下降,而NOS表达明显上调。结论:治疗剂量阿霉素能够降低心和肾组织中Ca~(2+)-ATP酶的活性和上调NOS的表达,是导致心和肾组织损伤的重要原因。

Heart and kidney injury caused by adriamycin and expression of nitric oxide synthase in rabbits

Objective : To study heart and kidney injury caused by adriamycin and expression of nitric oxide synthase in rabbits. Methods :Rabbits were intravenously injected with the therapeutic dosage of Adr as the cardiac muscule and kidney tissue injury model group. The cardiac output, left ventricle systolic pressure and left ventricle end diastolic pressure were measured. Cardiac muscular tissue and kidney tissue were collected from both groups. HE staining and enzyme histo-chemical staining were performed. Changes of the ATPase activity and NOS expression of cardiac muscular and kidney tissue from 2 groups were observed. Results :Compared with the control group, the cardiac output, left ventricle systolic-pressure were significantly decreased, but left ventricle end diastolic pressure was significantly increased in the experiment group; the cardiac muscular tissue and kidney tissue ultrastructures were harmed; Ca -ATPase activity descended and expression of NOS elevated. There were prominent differences between 2 groups. Conclusion : Therapeutic dosage of Adr descends Ca2+ -ATPase activity and elevates expression of NOS, which may be the important cause of cardiac muscular tissue and kidneys tissue injury.