摘要
目的 探讨再灌注时吸入一氧化氮 (NO)对兔肺一氧化氮合酶 (NOS)同功酶表达的影响 .方法 40只健康新西兰大白兔随机分成 4组 ,每组 10只 .假手术组 ( 组 ) ;假手术+吸入 NO组 ( 组 ) ;缺血再灌注组 ( 组 ) ;缺血再灌注 +吸入 NO组 ( 组 ) .通过阻断左肺门 6 0 min,随即阻断右肺门 ,造成左肺单侧再灌注 2 40 min. , 组在阻断右肺门前 5min吸入 5 0× 10 - 6NOppm.再灌注 2 40 min后 ,各组取左下叶组织 ,采用免疫组化方法检测再灌注肺 NOS同功酶表达变化 .结果 1 , 组肺组织未见 i NOS的表达 ,e NOS在内皮细胞表达正常 . 2 组内皮细胞、肺泡上皮细胞、平滑肌细胞等均可见大量 i NOS表达 (分别为 91.6 7%,83.3%和 81.6 %.与 相比 P<0 .0 5 ) ,e NOS表达下调 (5 6 .5 7%.与 相比 P<0 .0 5 ) . 组肺组织 i NOS表达受抑制 ,e NOS表达正常 .结论 1再灌注肺组织 e NOS表达减弱 ,i NOS表达增强 ,导致 NO合成增多 ,造成肺组织缺血灌注损伤 . 2吸入NO能抑制肺组织 i NOS表达 ,维持 e NOS在内皮细胞的正常表达 ,减轻肺再灌注损伤 .
AIM To evaluate the effect of nitric oxide synthase of inhaled nitric oxide on reperfused lung in rabbit model. METHODS Forty NewZealand rabbits were divided into four groups: group Ⅰ, sham-operated; group Ⅱ, sham-operated with inhaled nitric oxide; group Ⅲ, ischemia/reperfusion (I/R); group Ⅳ, I/R with inhaled nitric oxide. The rabbit model of reperfused lung injury was established by snaring the hilus of the left lung for 60 minutes and then releasing the snares to reperfuse only the left lung for 240 minutes. The expression of NOS was assayed by immunohistochemistry. RESULTS In the I/R lung (groupⅢ), strong expression of iNOS was seen in the endotheliul cells, alveolar epithelium and smooth muscle cells (91.67%, 83.3% and 81.6%, respectively. P<0.05 vs group Ⅰ) and the expression of eNOS was downregulated (56.57%. P<0.05 vs group Ⅰ). Inhaled nitric oxide inhibited iNOS expression with no effect on the expression of eNOS in the reperfused lung. CONCLUSION Inhaled nitric oxide downregulates iNOS immunoreactivity and has no effect on the expression of eNOS, which attentuates the reperfused lung injury.
出处
《第四军医大学学报》
CAS
北大核心
2002年第18期1641-1644,共4页
Journal of the Fourth Military Medical University
基金
福建省科委基金资助项目 ( 2 0 0 1z031)
福建省教育厅基金资助项目 ( K2 0 010 70 )
关键词
一氧化氮
再灌注
肺
一氧化氮合酶
nitric oxide
reperfusion
lung
nitric oxide synthase
