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Effects of inhaled nitric oxide on inflammatory mediators in rats with bacterial pneumonia
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- Author:
- No author available
- Journal Title:
- CHINESE JOURNAL OF EMERGENCY MEDICINE
- Issue:
- 6
- DOI:
- 10.3760/j.issn:1671-0282.2005.06.006
- Key Word:
- 肺炎克雷白杆菌;一氧化氮;肺炎
Abstract： 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1.3×108 cfu/只),然后分组(n=8～10)干预24h:吸入空气(PA)、NO(20×10-6,PNO)、低氧(FiO2 0.4,PLO)、低氧加NO(PLONO)、高氧(FiO2 1.0,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(TNF-α)和细胞间黏附分子-1(ICAM-1)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;TNF-α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);ICAM-1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TNF-α、ICAM-1、内皮细胞型NOS和iNOS mRNA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ICAM-1表达;吸入NO和/或低浓度氧可降低TNF-α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.
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