内源性一氧化氮与输胶体液过荷引起肺水肿关系的实验研究

Relationship between endogenous nitric oxide and pulmonary edema caused by overinfusion of colloid

目的:建立输胶体液过荷引起的肺水肿模型后,用NO合成酶抑制剂N~ω-硝基-L-精氨酸(L-NNA)和大剂量NO的生理性前体L-精氨酸(L-Arg),研究内源性NO与肺水的关系及对血液动力学和动脉血气的影响。方法:家免40只,随机分为:(Ⅰ) 空白对照组;(Ⅱ) 输液对照组:输血定安按一倍全血容量2ml·kg^(-1)·min^(-1);(Ⅲ) L-NNA组:输液前静注L-NNA 20mg/kg,(Ⅳ)L-Arg+L-NNA组:输液前静注L-Arg 300mg/kg。输液过程中监测MAP、HR、CVP;输液前、后作动脉血气析;实验完毕,测血NO含量及肺水指标。结果:输胶体液过荷时,L-NNA 20mg/kg使血中NO含量减少,血管外肺水(EVLW)增加,HR下降,CVP升高,SaO_2、PaO_2下降;L-精氨酸逆转了L-NNA的作用。血中NO值与EVLW呈负相关(r=-0.94),EVLW与总肺水呈正相关(r=0.414)。结论:内源性NO能缓解输胶体液过荷所致的肺水肿。

Objective: To investigate the role of endogenous nitric oxide (NO) in the pulmonary edema caused by overinfusion of colloid. Method: Forty healthy rabbits were randomly allocated into (Ⅰ) control group, (Ⅱ) infusion control group: one fold total blood volume of Gelofusine was infused at 2ml·kg^(-1)·min^(-1)(Ⅲ)L-NNA group:LNNA 20 mg/kg was intravenously injected before infusion, (Ⅳ)L-Arg+L-NNA group:L-arginine 300mg/kg and LNNA 20 mg/kg was intravenously injected before infusion. MAP,HR and CVP were recorded during the experiment, arterial blood gas analysis was examined before and after infusion,serumal NO value and lung water content were measured at the end of the experiment. Result: Overinfusion of colloid,L-NNA,an inhibitor of NO synthesis increased the extravascular lung water (EVLW) content and decreased NO value,meanwhile CVP increased,HR,PaO_2 and SaO_2 decreased,excess dose of L-arginine completely reversed the effect of L-NNA. Serumal NO value was negatively correlated with EVLW content (r=-0.94). EVLW content was significantly correlated with total lung water (r=0.41). Conclusion:Endogenous NO can reduce the pulmonary edema caused by overinfusion of colloid.