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目的 探讨杀菌 /通透性增加蛋白 ( BPI)对内毒素休克时血液动力学和内脏微循环灌注的保护作用及其机制。方法 采用大鼠内毒素休克模型 ,动态观察血液动力学、内脏微循环灌注量和血浆生物喋呤、一氧化氮 ( NO)水平的变化。结果 休克早期给予重组 BPI,可显著提高平均动脉压、心脏指数及每搏输出量 ,明显改善肝、肾、小肠微循环灌注量及动物预后 ( P<0 .0 5～ 0 .0 1) ;同时 ,治疗组血浆生物喋呤水平显著降低 ( P<0 .0 5～ 0 .0 1) ,循环 NO产生亦不同程度受到抑制。结论 早期应用 BPI能有效减轻内毒素休克时全身血液动力学紊乱及组织微循环障碍 ,该保护效应与 BPI抑制机体生物喋呤、NO的诱生相关。
Objective To investigate the protective effect of bactericidal / permeability-increasing protein (BPI) on hemodynamics and visceral microcirculation perfusion during endotoxic shock and its mechanism. Methods Rat endotoxic shock model was used to observe the hemodynamics, perfusion of visceral microcirculation and changes of plasma biopterin and nitric oxide (NO) levels. Results In the early stage of shock, administration of recombinant BPI significantly increased mean arterial pressure, cardiac index and stroke volume, and significantly improved the microcirculation perfusion and animal prognosis in the liver, kidney and small intestine (P <0.05-0.01). At the same time, the level of plasma biopterin in treatment group was significantly decreased (P <0.05-0.01), and the production of circulating NO was also inhibited to varying degrees. Conclusion Early application of BPI can effectively reduce systemic hemodynamic disturbances and tissue microcirculation during endotoxic shock. This protective effect is associated with the inhibition of BPI on the production of biopterin and NO.