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目的探讨吸入一氧化氮(NO)对肺炎克雷白杆菌肺炎大鼠肺部炎症介质的影响。方法健康大鼠随机分为肺炎组(P)和正常对照(C)组,P组气道注入肺炎克雷白杆菌(约1.3×108cfu只),然后分组(n=8～10)干预24h:吸入空气(PA)、NO(20×10-6,PNO)、低氧(FiO20.4,PLO)、低氧加NO(PLONO)、高氧(FiO21.0,PHO),高氧加NO(PHONO);C组吸入空气(CA)或NO(CNO)。测定肺组织原生型和诱生型NO合酶(cNOS和iNOS)活性,肿瘤坏死因子α(TNFα)和细胞间黏附分子1(ICAM1)蛋白水平及mRNA表达。结果PA组iNOS活性显著高于CA组(P<0.01),cNOS活性显著低于CA组(P<0.01);PNO、PLO、PLONO、PHO及PHONO组均可使被抑制的cNOS活性增强,PHO及PHONO可抑制iNOS活性增加;TNFα水平PA和PHONO组均显著高于CA组(P<0.01),PNO、PLO和PLONO组均显著低于PA组(P<0.01);ICAM1水平PA组显著高于CA组(P<0.01),PNO、PLONO和PHONO组分别低于PA、PLO和PHO组(P<0.01)。各组肺组织TNFα、ICAM1、内皮细胞型NOS和iNOSmRNA表达差异均无显著性。结论吸入NO和或氧气对肺炎大鼠肺内cNOS及iNOS活性具有不同调节作用;吸入NO可抑制肺组织ICAM1表达;吸入NO和或低浓度氧可降低TNFα表达。吸入NO可能通过调节急性炎症反应介质预防炎症性肺损伤。
Objective To investigate the effects of inhaled nitric oxide (NO) on pulmonary inflammatory mediators in Klebsiella pneumoniae with pneumonia. Methods Healthy rats were randomly divided into pneumonia group (P) and normal control group (C). P group was challenged with Klebsiella pneumoniae (about 1.3 × 108cfu only), and then were divided into groups (n = 8-10) Inhalation air (PA), NO (20 × 10-6, PNO), low oxygen (FiO20.4, PLO), low oxygen plus NO (PLONO), high oxygen (FiO21.0, PHO) PHONO); Group C inhaled air (CA) or NO (CNO). The activity of primary and induced NO synthase (cNOS and iNOS) and the expression of tumor necrosis factor alpha (TNFα) and intercellular adhesion molecule 1 (ICAM1) protein and mRNA in lung tissue were measured. Results The iNOS activity of PA group was significantly higher than that of CA group (P <0.01) and cNOS activity was significantly lower than that of CA group (P <0.01). The activity of cNOS was inhibited by PNO, PLO, PLONO, PHO and PHONO groups, (P <0.01). The levels of TNFα in both PA and PHONO groups were significantly higher than those in CA group (P <0.01), while those in PNO, PLO and PLONO groups were significantly lower than those in PA group (P <0.01) In CA group (P <0.01), PNO, PLONO and PHONO groups were lower than those in PA, PLO and PHO groups (P <0.01). There was no significant difference in the expressions of TNFα, ICAM1, NOS and iNOS mRNA in lung tissue among all groups. CONCLUSION: NO and / or oxygen inhalation can regulate the cNOS and iNOS activity in lungs of rats with pneumonia. Inhalation of NO can inhibit the expression of ICAM1 in lung tissue. Inhaled NO and / or low concentration of oxygen can decrease the expression of TNFα. Inhalation of NO may prevent inflammatory lung injury by modulating acute inflammatory response mediators.