Acta Pharmacologica Sinica (2009) 30: 1643–1647; doi: 10.1038/aps.2009.161

 
Original Article
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A novel acute anemia model for pharmacological research in mice by compelled acute exercise
 

Qing-shan LIU2, #, Jin-hua WANG1, #, Jian CUI2, Zhi-hong YANG1, 3, Guan-hua DU1,*

1Institute of Materia Medica, Chinese Academy of Medical Science & Peking Union Medical College, Beijing 100050, China; 2National Research Center for Chinese Minority Nationality Medicine, Minzu University of China, Beijing 100081, China; 3Institute of Medicinal Plant Development, Chinese Academy of Medical Science & Peking Union Medical College, Beijing 100050, China

 

Aim: To generate a novel acute anemia model by compelled exercise.

 

Methods: Young adult male mice were compelled to perform an acute exercise by electric stimulation for 30 min.  Blood was taken from their tails to be used for detection immediately after exercise.

 

Results: It was found that the red blood cell (RBC) count, hemoglobin concentration and hematocrit of exhausted mice were lower than that of sedentary mice without electric stimulation.  The model is in line with the diagnostic criteria.  As the mechanisms of the acute anemia model, it was found that the osmotic fragility of the RBC in model mice increased compared to that of normal mice, and that the deformation index, orientation index, small deformation index, deformability and orientation of RBCs in the model mice were reduced.  The glutathione (GSH) levels in blood plasma were decreased.  The liver, spleen, kidney had no detectable changes.


Conclusion:
To the best of our knowledge, these effects represent the success of a novel anemia model by compelled acute exercise.  The oxidative damages on RBC and hemorheological changes are in part the causes of acute anemia in this model.

 

Keywords: anemia; mice; hemorheology; hematocrit; hemoproteins

 

Experimental works conducted in the authors’ laboratories were supported by Chinese High Technological Project (No 2004AA2Z3782) and National Natural Science Foundation (No 0630073, 30973959).

# These authors contribute equally to this work.
* To whom correspondence should be addressed.
E-mail dugh@imm.ac.cn  
Received 2009-03-14    Accepted 2009-09-29

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