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目的观察油酸肺损伤早期肺组织一氧化氮合成酶（ＮＯＳ）活性变化、诱导型一氧化氮合成酶（ｉＮＯＳ）基因表达变化及其细胞定位。方法３Ｈ－胍氨酸测定法测定ＮＯＳ活性；应用３２Ｐ标记核酸探针狭线杂交技术和地高辛标记核酸探针原位杂交技术检测油酸肺损伤大鼠肺组织。结果正常肺组织ＮＯＳ活性很低且无ｉＮＯＳｍＲＮＡ表达；急性肺损伤后ｉＮＯＳ活性升高且与ｉＮＯＳｍＲＮＡ表达相一致；硝基左旋精氨酸（ＬＮＮＡ）可抑制ｉＮＯＳ活性并下调ｉＮＯＳｍＲＮＡ表达；伤后表达ｉＮＯＳｍＲＮＡ的阳性细胞可能为肺泡巨噬细胞、粒细胞、支气管上皮细胞、肺泡上皮细胞、平滑肌细胞、内皮细胞。结论急性肺损伤后肺组织ｉＮＯＳｍＲＮＡ的表达是一个突然启动的主动合成过程；ＬＮＮＡ抑制ＮＯ产生可能与其下调ｉＮＯＳｍＲＮＡ表达有关；肺组织表达ｉＮＯＳｍＲＮＡ阳性细胞的多样性可能与ＮＯ损伤肺组织的复杂性有关。
Objective To observe the change of lung tissue nitric oxide synthase (NOS) activity and the expression of inducible nitric oxide synthase (iNOS) gene in early oleic acid induced lung injury and its cellular location. Methods The activity of NOS was determined by 3H-citrulline assay. The lung tissues of rats with oleic acid-induced lung injury were detected by the 32P-labeled nucleic acid probe and the digoxigenin-labeled nucleic acid probe in situ hybridization. Results NOS activity in normal lung tissue was low and no iNOS mRNA expression was found. The iNOS activity was increased and consistent with iNOS mRNA expression in acute lung injury. Nitro-L-arginine (LNNA) inhibited iNOS activity and down-regulated the expression of iNOS mRNA and iNOS mRNA The positive cells may be alveolar macrophages, granulocytes, bronchial epithelial cells, alveolar epithelial cells, smooth muscle cells, endothelial cells. Conclusions The expression of iNOS mRNA in lung tissue after acute lung injury is an abrupt initiating active synthesis process. LNNA inhibits the production of NO possibly related to the down-regulation of iNOS mRNA expression. The diversity of iNOS mRNA positive cells in lung tissue may be related to the complexity of lung tissue damaged by NO.