骨筋膜室综合征神经功能和结构改变的研究  

Pathogenesis and therapeutic effect of ketoprofen in pulmonary damage caused by intraabdominal infection

作　　者：彭昊[1] 李家元[1] 黄琪裳 王炳勋 

机构地区：[1]湖北医科大学附属第一医院骨科,武汉430060

出　　处：《中华实验外科杂志》1996年第2期117-118,共2页Chinese Journal of Experimental Surgery

摘　　要：采用骨筋膜室综合征动物模型,在25条犬后肢观察前外侧骨筋膜室组织液压增高对腓深神经传导功能及组织结构的影响。结果发现,当室内液压为4kPa维持4～6小时,其神经传导速度减慢有显著性差异(P<0.01)。出现不完全性传导阻滞,光、电镜检查显示神经轴突肿胀,轴突内结构肿胀变性及脱髓鞘改变。室内液压在6.67kPa或以上即可导致完全性传导阻滞,且压力越高,完全阻滞所需时间越短,轴突变性及脱髓鞘越明显。实验结果有助于确定骨筋膜室综合征切开减压的临界压(4kPa)及临界时间(4～6小时),尤其对合并意识丧失和脊髓损伤的病例有一定的指导意义。The pathogenesis and the therapeutic effect of ketoprofen upon pulmonary damage induced by intraabdominal infection were investigated in rabbits. The increase of pulmonary extravascular water volume (PEWV) and pulmonary capillary permeability occurred in early phase of intraabdominal infection (oecal ligation and perforation, CLP), 12 h after CLP. PaO_2 and SatO_2 in arteria decreased significantly. The levels of serum endotoxin, 6-keto-PGF_(10) and TXB_2 significantly increased. TXB_2 was strongly correlated with degrees of pulmonary edema. 6 h after CLP, the venoclysis of detoprofen was able to decrease the capillary permeability and PEWV. However. 12 hafter CLP, the therapeutic effect of ketoprofen diminished. When the dosage of ketoprofen was increased, no obvious change of the pulmonary edema was observed.

关 键 词：骨筋膜室综合征 神经功能 神经结构 

分 类 号：R681.202[医药卫生—骨科学]