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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。
Objective: To investigate the effects of adriamycin on heart and kidney injury and nitric oxide synthase (NOS) expression. METHODS: Rabbit model of heart and kidney injury was established by intravenous injection of doxorubicin. The cardiac output (CO), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP) Tissues were stained with HE and ultrathin sections. NADPH staining and image analysis were performed to observe the changes of ALP, Ca ~ (2 +) - ATPase and NOS in heart and kidney of animals. Results: The levels of CO and LVSP in the experimental group were significantly lower than those in the control group, and the LVEDP level was significantly higher in the experimental group than that in the control group. The ultrastructure of heart and kidney tissue were damaged and the activity of Ca ~ (2 +) - ATPase was significantly decreased Significantly increased. Conclusion: The therapeutic dose of doxorubicin can reduce the activity of Ca ~ (2 +) - ATPase in heart and kidney and upregulate the expression of NOS, which is an important cause of heart and kidney damage.