Study on the mechanisms of pathogenesis of critical illness polyneuropathy and protective effect of activated factor X.

采用实时荧光定量聚合酶链式反应方法检测了脓毒症所致重症多发性神经病大鼠模型(L组)坐骨神经8种电压依赖性钠通道受体亚型(NAV)的表达，并与对照组(C组)进行比较。结果显示，与C组相比，L组三种不同类型NAV的基因表达显著降低，而三种不同类型NAV的基因表达显著增加。这些结果提示不同类型的钠通道基因表达在作为通道病的危重病多发性神经病的发病机制中起重要作用。由于药物X和/或药物Y的应用不能改善NAV基因表达的改变，药物X和药物Y的其他作用可能参与了脓毒症时神经功能的改善。

We measured the expression of eight kinds of voltage-dependent sodium channel receptor subtypes (Nav) of the sciatic nerve by the real-time PCR method in sepsis induced critical illness polyneuropathy rat model (L-group) and compared to the control group (C-group). We achieved the results shown the significant reductions of gene expression in three subtypes of Nav and increases in three different kinds of Nav in L-group compared to C-group. These data implied the different types of sodium channel gene expression plays an important role in the mechanisms of pathogenesis of critical illness polyneuropathy as channelopathy.Since the administration of Drug-X and/or Drug-Y did not improve the alteration in Nav gene expression, other actions of Drug-X and Drug-Y might be involved in the improvement of nerve function during sepsis.