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Effect of low molecular weight heparin on neural function after cardiopulmonary resuscitation in rabbits |
GUAN Zeng- gan, XIE Yong- peng, WANG Yan- li, LIU Ke- xi |
Department of Intensive Care Unit, Lianyungang Hospital of Xuzhou Medical University, Lianyungang 222002, China |
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Abstract Objective To explore the effects of low molecular weight heparin(LMWH)on Creactive protein(CRP), high mobility group box- 1 protein(HMGB-1), S100B and neurons injury in hippocampus CA1 region after cardiopulmonary resuscitation in rabbits. Methods Thirty rabbits were randomly divided into three groups: Sham operation group(Sham group), Control group(Con group),LMWH treatment group (LMWH group). Rabbits were anaesthetized with pelltobarbitalu natricum.After anaesthetization, trachea was exposed and intubated, and then right femoral artery was cannulated for monitoring of blood pressure and blood samples taken. Animals in Con group and LMWH group under⁃wentendotracheal tube clamping to induce cardiac arrest; epinephrine without or with LMWH were given during the cardiopulmonary resuscitation respectively. Blood samples were taken before, and 0, 2, 6, 12,24, 48 hour after return of spontaneous circulation(ROSC)for detection of the concentrations of CRP,HMGB-1, S100B in the serum. Rabbits were decapitated 48 hour after ROSC, hippocampus was taken for the hematoxylin-eosin staining test. Results In comparison with Sham group, the concentrations of CRP, HMGB-1, S100B in Con group and LMWH group were significantly increased after ROSC(P<0.05), neuronal cells in hippocampus CA1 region were shrinkage and nuclei were pyknotic. In comparison with Con group, S100B in LMWH group was decreased after ROSC (P < 0.05), CRP,HMGB-1 were decreased since 2 hour after ROSC in LMWH group, and neurons injury in hippocampus CA1 region was less. Conclusion LMWH can inhibit the inflammation after cardiopulmonary resuscitation, decrease the concentration of S100B in the serum, and attenuate the cerebral injury.
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Received: 02 February 2016
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Corresponding Authors:
LIU Ke-xi, E-mail: liukexi2006@163.com
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