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    M echan ism s of Dexametha sone to Protect Flaps

    from an Ischem ia-Reperfus ion In jury

    CAO J ingm in LU Kaihua GUO Shuzhong

    【Abstract】 Object ive To study the effect of dexamethasone to p ro tect f lap s f rom an ischem ia2reperfusion

    injury and elucidate itsmechanism of regulat ing the death course of the neut roph ils . Methods The ratsw ere random ly

    divided into 3 group s . The vein of the rat w as clamped fo r 8 h af ter the f lap had fo rmed . Group A: the no rmal f lap;

    Group B: the saline cont ro l f lap; Group C: the t reatment f lap w ith dexamethasone . The survival area of the f lap s w as

    measured at 7 days; the apop to t ic and necro t ic neut roph ils, tumo r necro sis facto r A (TN F2A ) , and inter leuk in 10 ( IL 2

    10) concent rat ionsw ere measured . Results The f lap survival areas in Group sA and C w ere larger than tho se in Group

    B. The apop to t ic neut roph ils in Group B w ere few er than tho se in Group s A and C on the 1st and 3rd days af ter

    operat ion; how ever, they w ere mo re in number in Group B than in group sA and C on the 6th day . The necro t ic cells in

    Group B w eremo re in number than tho se in Group sA and C. In Group B, the p lasma TN F2Aconcent rat ion reached the

    maximum level at 1 h, w h ile the IL 210 level reached the low est 3 h af ter the reperfusion . In Group C, the TN F2A

    concent rat ion w as low er than that in Group B and decreased dramat ically at 6 h. The IL 210 concent rat ionw as the low est

    at 1 h, and increased rap idly at 3 h. Thus, ischem ia2reperfusion could injure the f lap s, p robably th rough the abno rmal

    act ion of the neut roph ils, such as the diso rdered secret ion of the cytok ines and abno rmal death course of the

    neut roph ils . Conclus ion Dexamethasone can p ro tect the f lap f rom an ischem ia2reperfusion injury by its regulat ion fo r

    the neut roph il funct ion .

    【Key words】 F lap Ischem ia2reperfusion injury Dexamethasone

    INTRODUCTION

    The adhesion of the neu t roph ils to the vascu lar

    endo thelial cells accoun t s fo r one of the m echan ism s

    by w h ich the island f lap s w ill suffer f rom an

    ischem ia2reperfu sion in ju ry

    [ 1 ]

    . The t reatm en t of an t i2

    adhesion of the neu t roph ils to the endo thelium , such

    as a u se of monoclonal an t ibody of CD11a? CD18 o r

    CD11b? CD18, has m ade som e p rogress in p reven t ing

    the f lap f rom necro sis

    [ 2 ]; how ever, such good resu lt s

    have no t been ach ieved clin ically . That m ean s that,besides the abno rm al adhesion of the neu t roph ils,o ther neu t roph il act ion s, such as abno rm al death

    p rocess (apop to sis and necro sis) and the diso rdered

    secret ion of cytok ines, have p layed an impo r tan t ro le

    in the ischem ia2reperfu sion in ju ry to the f lap.

    How ever, th is impo r tan t m echan ism has no t draw n

    the concern of the scho lars . Therefo re, w e studied

    the m echan ism of dexam ethasone to p reven t the f lap s

    f rom the ischem ia2reperfu sion in ju ry, and found the

    Department of P last ic Surgery, Xi J ing Ho sp ital, Fourth M ilitary

    M edical U niversity, Xi’an Shannxi, 710032, P. R. Ch ina

    Co rresponding autho r: CAO J ingm in, ch ief physician, Department

    of P last ic Surgery, Xi J ing Ho sp ital, Fourth M ilitary M edical

    U niversity, Xi’ an Shaanxi, 710032, P. R. Ch ina . E2 mail : jingm incao ......

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