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Chinese Archives of General Surgery(Electronic Edition) ›› 2011, Vol. 05 ›› Issue (03): 206-210. doi: 10.3877/cma.j.issn.1674-0793.2011.03.007

Special Issue:

• Original Article • Previous Articles     Next Articles

Protective effects of exogenous phosphocreatine on myocardial damage induced by hemorrhagic shock and its mechanisms

qin ZHOU1, Qing-chun LIANG1, Peng YANG1, Xiao-yun DUAN1, Wen-qi HUANG1()   

  1. 1. Department of Anesthesiology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China
  • Received:2010-12-21 Online:2011-06-01 Published:2011-06-01
  • Contact: Wen-qi HUANG
  • About author:
    Corresponding Author: HUANG Xiong-qing, Email:

Abstract:

Objective

To observe protective effects of exogenous phosphocreatine on myocardial damage induced by hemorrhagic shock and its mechanisms.

Methods

Twenty healthy white rabbits were randomly divided into Control group (Group N) and Exogenous Phosphocreatine group (Group CP). Acute hemorrhagic shock animal model was established according to Wigger’s method. The changes of mean arterial pressure (MAP), serum creatine phosphokinase(CK) and cardiac Troponin I (cTn-I), myocardial mitochondrial ATPase, apoptosis and myocardial morphological structure were observed.

Results

There were excessive myocardial injuries in Group N, while in Group CP the myocardial myofilament disarray and the pathological finding were not as severe as in Group N. Compared with the group N, the level of CK and cTnI significantly decreased during reperfusion, the activity of mitochondrial Na+-K+-ATPase and Ca2+-ATPase significantly increase and the total number of staining myocytes of CP group were lower(P<0.05).

Conclusion

CP can protect markedly the myocardial damage induced by hemorrhagic shock.

Key words: Exogenous phosphocreatine, Hemorrhagic shock, Energy metabolism, Mitochondrial injury, Apoptosis

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