分子生物学研究初步阐明 ,感染性休克是细菌内毒素诱导炎症介质瀑布样连锁反应 ,导致循环功能衰竭的结果。一氧化氮 (ＮＯ)是最终的共同关键介质之一 ,直接参与感染性休克的发生发展[1～ 2 ] 。因此 ,抑制ＮＯ的异常大量合成和释放 ,封闭其活性 ,一度成为感染性休克的重要治疗 Molecular biology initially clarified that septic shock is a bacterial endotoxin-induced inflammatory cascade waterfall-like chain reaction, leading to circulatory failure results. Nitric oxide (NO) is one of the final common key mediators, and is directly involved in the development of septic shock [1-2]. Therefore, inhibiting the abnormal synthesis and release of NO in large quantities and blocking its activity became an important treatment for septic shock