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急性肾损伤
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    Conclusion Renal damage could be induced by exhaustive swimming, the main type of the damage was renal tissue cell apoptosis.
    结论过度训练可引起急性肾损伤,肾组织细胞凋亡是其损伤的主要表现形式;
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  acute renal injury
After acute renal injury, renal expression of several growth factors becomes transiently altered.
      
The data indicate thatCCr is not an accurate indicator of GFR in children who have had acute renal injury.
      
It is reported that urinary annexin V concentration may be an indicator of apoptosis and acute renal injury related to the urinary protein level.
      
Reactive oxygen species (ROS) have been postulated to play a major role in postischemic acute renal injury.
      
Insulin-like growth factor-I increases p21 expression and attenuates cisplatin-induced acute renal injury in rats
      
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Objective To study the feature of renal damage induced by overtraining and the protective effect of anisodamine on the damage. Methods The animal model of renal damage induced by overtraining was developed by exhaustive swimming.The changes of renal function were measured.The renal tissue structure was observed by Olympus microscopy.The renal cell apoptosis was observed by teninal-deoxynucleotidy transferase mediatedd-dUTPnick end labeling. Results The serum biochemical parameters, such as Ur and CK increased...

Objective To study the feature of renal damage induced by overtraining and the protective effect of anisodamine on the damage. Methods The animal model of renal damage induced by overtraining was developed by exhaustive swimming.The changes of renal function were measured.The renal tissue structure was observed by Olympus microscopy.The renal cell apoptosis was observed by teninal-deoxynucleotidy transferase mediatedd-dUTPnick end labeling. Results The serum biochemical parameters, such as Ur and CK increased immediately after exhausted rat. It was more prominent at 6 hour and recovered to the normal at 24 hour. γ-GT in the urine was increased at l2 and 24 hour after exhausted rat. The morphologic changes were slight under light microscopy in HE staining. It was revealed by TUNEL that the number of apoptotic cell was increased in kidney of rats afrer exhaustive swimming, especially at 24 hour. After using of Anisodamine, compared with that of control rats, time of swimming was prolonged significantly, renal function was improved, no morphologic changes can be found, the number of renal tissue apoptotic cells was decreased remarkably.Conclusion Renal damage could be induced by exhaustive swimming, the main type of the damage was renal tissue cell apoptosis. Anisodamine had the protective effect on the damage.

目的研究过度训练致急性肾损伤的特点及山莨菪碱的保护作用。方法采用大鼠游泳至力竭建立过度训练致急性肾损伤模型。将大鼠随机分为7组,即安静对照组、力竭即刻组、力竭6h组、力竭12h组、力竭24h组、山莨菪碱6h组、山莨菪碱24h组,用全自动生化仪检测各组大鼠血Cr、Ur、CK及尿γ-GT的改变;光镜观察各组肾组织结构的改变;用TUNEL法检测各组大鼠肾组织细胞凋亡,采用图像分析仪计算肾组织细胞凋亡率。结果力竭后大鼠站立不稳,对声光刺激反应淡漠。力竭后即刻组大鼠血Ur、CK明显升高(P<0.05),力竭6h后血Ur、CK继续升高(P<0.01),力竭12h后血Ur、Cr、CK均有所下降,尿γ-GT明显升高(P<0.01),力竭24h后血Ur、Cr、CK均恢复到正常,尿γ-GT继续升高(P<0.01)。光镜下力竭后即刻组大鼠肾组织结构仅见部分肾小球囊及肾小管扩张,在皮髓质交界处及髓质小血管内可见大量红细胞堆积,力竭12h大鼠可见肾小管上皮细胞刷状缘不规整,部分脱落,肾小管管腔内可见颗粒管型和透明管型,在皮髓质交界处及髓质可见大量细胞核深染,有固缩现象;力竭后即刻、6、12、24h组大鼠肾组织凋...

目的研究过度训练致急性肾损伤的特点及山莨菪碱的保护作用。方法采用大鼠游泳至力竭建立过度训练致急性肾损伤模型。将大鼠随机分为7组,即安静对照组、力竭即刻组、力竭6h组、力竭12h组、力竭24h组、山莨菪碱6h组、山莨菪碱24h组,用全自动生化仪检测各组大鼠血Cr、Ur、CK及尿γ-GT的改变;光镜观察各组肾组织结构的改变;用TUNEL法检测各组大鼠肾组织细胞凋亡,采用图像分析仪计算肾组织细胞凋亡率。结果力竭后大鼠站立不稳,对声光刺激反应淡漠。力竭后即刻组大鼠血Ur、CK明显升高(P<0.05),力竭6h后血Ur、CK继续升高(P<0.01),力竭12h后血Ur、Cr、CK均有所下降,尿γ-GT明显升高(P<0.01),力竭24h后血Ur、Cr、CK均恢复到正常,尿γ-GT继续升高(P<0.01)。光镜下力竭后即刻组大鼠肾组织结构仅见部分肾小球囊及肾小管扩张,在皮髓质交界处及髓质小血管内可见大量红细胞堆积,力竭12h大鼠可见肾小管上皮细胞刷状缘不规整,部分脱落,肾小管管腔内可见颗粒管型和透明管型,在皮髓质交界处及髓质可见大量细胞核深染,有固缩现象;力竭后即刻、6、12、24h组大鼠肾组织凋亡细胞数逐渐增多,多位于皮髓质交界处及髓质的肾小管和集合管,各组大鼠尿γ-GT与肾组织细胞凋亡率有明显相关性(P<0.01)。应用山莨菪碱后,力竭大鼠精神状态较好,游泳时间明显延长(P<0.01);力竭后6h及24h血Ur、Cr、CK及尿γ-GT均明显降低(P<0.05),肾组织结构改善,肾组织凋亡细胞数明显减少。结论过度训练可引起急性肾损伤,肾组织细胞凋亡是其损伤的主要表现形式;山莨菪碱可提高运动能力,同时可减少肾组织细胞凋亡,进而对肾损伤起到明显的保护作用。

 
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