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肢体缺血/再灌注后急性肺损伤中未特指的表达及其在大鼠中的意义

[Expression NOS in acute lung injury following limb ischemia/reperfusion and its significance in rats].

作者信息

Zhang Yi-Bing, Zhang Lian-Yuan, Men Xiu-Li, Dong Shu-Yun, Yang Quan-Hui, Yao Rui-Li

机构信息

North China Coal Medical College, Tangshan 063000, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2006 Nov;22(4):484-7.

PMID:21155281
Abstract

AIM

To investigate the expression and role of inducible NOS (iNOS) and endothelial NOS (eNOS) in acute lung injury following limb ischemia/reperfusion (4h/4h).

METHODS

Wistar rats were randomized into four groups: control group, ischemia/reperfusion (I/R) group, L-Arginine (L-Arg) pretreatment group, Aminoguanidine (AG) pretreatment group. The lung tissue of each group was subjected to assay of content of MDA, MPO, W/D and NO2-/NO3-. The expression of iNOS and eNOS was examined with immunohistological staining. The pulmonary morphologic changes were observed under microscope respectively.

RESULTS

The acute lung injury existed after limb ischemia/reperfusion. The eNOS downregulation and iNOS upregulation among I/R, L-Arg and AG groups were observed contrasted to the control group. There was no expressional and statistical difference of iNOS between I/R group and L-Arg group. The expression of eNOS was similar between IR and AG but iNOS expression was downregulated in AG. The parameters of MDA, MPO, W/D and NO2-/NO3- in pulmonary tissue were significantly increased in I/R groups compared with those of the control group. The parameters of L-Arg and AG pretreatment groups in comparison with those of the I/R group showed significantly difference. Based on the results of pulmonary pathology, the congestion and infiltration of inflammatory cells existed obviously in IR group. L-Arg played definite role in militating lung injury and AG might make lung injury aggravated.

CONCLUSION

The NO definite production from iNOS is possible to play a competitivly protective role in acute lung injury following limb ischemia/reperfusion and antagonist of iNOS may aggravate the lung injury.

摘要

目的

研究诱导型一氧化氮合酶(iNOS)和内皮型一氧化氮合酶(eNOS)在肢体缺血/再灌注(4小时/4小时)后急性肺损伤中的表达及作用。

方法

将Wistar大鼠随机分为四组:对照组、缺血/再灌注(I/R)组、L-精氨酸(L-Arg)预处理组、氨基胍(AG)预处理组。检测每组肺组织中丙二醛(MDA)、髓过氧化物酶(MPO)、湿干比(W/D)及亚硝酸盐/硝酸盐(NO2-/NO3-)含量。采用免疫组织化学染色检测iNOS和eNOS的表达。分别在显微镜下观察肺组织形态学变化。

结果

肢体缺血/再灌注后存在急性肺损伤。与对照组相比,I/R组、L-Arg组和AG组中eNOS表达下调,iNOS表达上调。I/R组和L-Arg组之间iNOS的表达和统计学上无差异。IR组和AG组中eNOS的表达相似,但AG组中iNOS表达下调。与对照组相比,I/R组肺组织中MDA、MPO、W/D及NO2-/NO3-参数显著升高。L-Arg预处理组和AG预处理组与I/R组相比,参数有显著差异。基于肺病理学结果,IR组中炎症细胞的充血和浸润明显存在。L-Arg在减轻肺损伤方面发挥了一定作用,而AG可能会加重肺损伤。

结论

iNOS产生的一氧化氮(NO)可能在肢体缺血/再灌注后的急性肺损伤中发挥竞争性保护作用,iNOS的拮抗剂可能会加重肺损伤。

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