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目的：探讨一氧化氮（NO）在感染性休克中的作用机制，及抑制NO合成的治疗学意义。方法：10只健康杂种狗予戊巴比妥麻醉，大肠杆菌内毒素（LPS）60μg·kg-1·h-1×30min静脉滴注，继以生理盐水（NS）15ml·kg-1·h-1维持。随机分成两组。组Ⅰ、组Ⅱ在LPS开始注射后60min分别单剂注射NS30ml、NS30ml＋L-硝基精氨酸（LNNA）20mg·kg-1。观察血液动力学、氧动力学、尿NO3/NO2（NOx）、血浆内皮素（ET）变化。结果：LPS注射后60min两组动物均呈典型高动力状态，平均动脉压（MAP）、体循环阻力（SVRI）明显下降，心脏指数（CI）轻度增加。LPS使氧输送（DO2）、氧耗（VO2）增加。尿NOx升高。LNNA使MAP恢复至基础水平，SVRI、PVRI显著升高且超过基础值；CI下降，DO2、VO2减少，PvO2上升，尿NOx低于组Ⅰ，而ET明显高于组Ⅰ。结论：LPS诱导的犬感染性休克的血液动力学异常与NO过多释放有关，NO抑制LPS引起的ET释放。LNNA虽可逆转低血压，但对感染性休克的整体治疗不利。
Objective: To investigate the mechanism of action of nitric oxide (NO) in septic shock and the therapeutic significance of inhibiting NO synthesis. Methods: Ten healthy mongrel dogs were anesthetized with pentobarbital, 60μg · kg-1 · h-1 × 30min of E. coli lipopolysaccharide (LPS) was given intravenously, followed by saline 15ml · kg-1 · h -1 to maintain. Randomly divided into two groups. Groups Ⅰ and Ⅱ were injected with NS30ml and NS30ml + LNNA 20mg · kg-1 respectively 60min after LPS injection. The changes of hemodynamics, oxygen dynamics, urinary NO3 / NO2 (NOX) and plasma endothelin (ET) were observed. RESULTS: At 60 minutes after LPS injection, both animals showed a typical high dynamic state. Mean arterial pressure (MAP) and systemic circulation resistance (SVRI) decreased significantly and cardiac index (CI) increased slightly. LPS oxygen delivery (DO2), oxygen consumption (VO2) increased. Urine NOx increased. LNNA restored the basal level of MAP, SVRI and PVRI increased significantly and exceeded the baseline value; CI decreased, DO2 and VO2 decreased, PvO2 increased, urinary NOX was lower than that of group Ⅰ, but ET was significantly higher than that of group Ⅰ. CONCLUSION: The hemodynamic abnormalities induced by LPS in septic shock in dogs are related to the excessive release of nitric oxide, and NO inhibits ET release induced by LPS. Although LNNA can reverse hypotension, it is not good for the overall treatment of septic shock.