| 急性肾功能衰竭家兔心肌损伤的体液机制 |
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| 引用本文： | 侯亚利,赵自刚,牛春雨,刘艳凯,姜华,张玉平,樊贵,张静.急性肾功能衰竭家兔心肌损伤的体液机制[J].河北北方学院学报(医学版),2006,23(2):1-3. |
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| 作者姓名： | 侯亚利 赵自刚 牛春雨 刘艳凯 姜华 张玉平 樊贵 张静 |
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| 作者单位： | 1. 河北北方学院附属第一医院检验科,河北,张家口,075000
2. 河北北方学院病理生理教研室,河北,张家口,075000 |
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| 基金项目： | 河北省科学技术研究与发展计划 |
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| 摘 要： | 目的：观察急性肾功能衰竭（ARF）家兔心肌匀浆自由基、一氧化氮的变化，探讨心肌损伤的体液机制。方法：60只家兔均分为四组（n=15）。ARF模型1组：皮下注射1％HgCl2（1．3ml／kg．bw）；ARF模型2组：肌肉注射50％甘油（10ml／kg．bw）；以等量生理盐水代替HgCl2和甘油作为对照1、2组。24h后，所有动物颈总动脉放血备检，并选择固定位置。制备10％心肌匀浆。经Aeroset型全自动生化分析仪测定血清反映肾功能的生化指标。检测心肌匀浆丙二醛（MDA）、超氧化物歧化酶（SOD）、一氧化氮（NO）及其合酶（NOS）的变化。结果：与相应对照组比较，ARF模型1、2组心匀浆SOD活性下降、MDA含量升高（P〈0．05），ARF模型1、2组心匀浆NO含量增强、NOS及iNOS活性增强（P〈0．05～0．01）。结论：ARF家兔心肌损伤的机制与自由基损伤及NO升高有关。
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| 关 键 词： | 急性肾功能衰竭 自由基 一氧化氮 心肌 |
| 文章编号： | 1673-1484(2006)02-0001-03 |
Humoral Mechanism of Myocardium Injury in Rabbits with Acute Renal Failure |
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| HOU Ya-li,ZHAO Zi-gang,NIU Chun-yu,et al.Humoral Mechanism of Myocardium Injury in Rabbits with Acute Renal Failure[J].Journal of Hebei North University:Medical Edition,2006,23(2):1-3. |
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| Authors: | HOU Ya-li ZHAO Zi-gang NIU Chun-yu |
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| Institution: | HOU Ya-li,ZHAO Zi-gang,NIU Chun-yu,et alDepartment of Clinical Laboratory,the First Affiliated Hospital,Hebei North University,Zhangjiakou 075000,Hebei China |
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| Abstract: | Objective:To observe the changes of free radical and nitric oxide(NO) in heart homogenate of rabbits with acute renal failure(ARF),and inquire into the humoral mechanism of myocardium injury.Methods:Sixty rabbits were divided into four groups(15 rabbits one group averagely).The ARF model group 1 was established by hypodermic injection 1% HgCl_(2)and injected amount was 1.3ml/kg.bw,and the ARF model group 2 was established by intramuscular injection 50% glycerinum and injected amount was 10 ml/kg.bw.The control group 1 and 2 were injected by equivalent volume of normal saline.After 24 hours,all rabbits were cannulated to draw out blood with drawal for serum sample,and taken out heart for making 10 percent homogenate.The biochemical indexes of renal function in serum were determined by Aeroset type automatic biochemical analyzer and so the superoxide dismutase(SOD),malondialdehyde(MDA),NO,nitric oxide synthase(NOS) and inducible nitric oxide synthase(iNOS) in heart homogenate were determined.Results:It showed that SOD activity was significantly lower and the MDA,NO,NOS and iNOS were significantly increased in heart homogenate of ARF group 1 and 2 compared with control group 1 and 2(P<0.01~0.05).Conclusion:There was myocardium damage in ARF,and its mechanism might be related with free redical-injure and NO-increase. |
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| Keywords: | Acute Renal Failure(ARF) Free redical Nitric oxide(NO) Myocardium |
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