【摘要】 将大鼠肺组织切片与香烟烟雾提取物（ＣＳＥ）共同孵育，测定其乳酸脱氢酶（ＬＤＨ）活性、亚硝酸盐（ＮＯ_２） 含量、一氧化氮合酶（ＮＯＳ）活性及左旋精氨酸（Ｌ－Ａｒｇ）转运，以探讨吸烟对肺组织的氧化损伤作用及对一氧化氮 生成的影响。结果显示： １０％ ＣＳＥ时间依赖地增加大鼠肺组织 ＬＤＨ漏出及 ＮＯ_２释放，二者高度正相关（ｒ=０．６５， Ｐ＜０．０１），刺激诱导型ＮＯＳ（ｉＮＯＳ）活性增加，并通过增加最大转运速度（Ｖｍａｘ）使Ｌ－Ａｒｇ转运增加。提示：吸烟可 能通过增加 Ｌ－Ａｒｇ的跨膜转运使细胞内 Ｌ－Ａｒｇ浓度增高，并增加 ｉＮＯＳ活性使 ＮＯ过量产生。 ＮＯ可能参与了吸烟对肺 组织的损伤过程。更多还原

【Abstract】 To evaluate the effects of cigarette smoking on lung tissue. The rat lung slices were incubated with 10% cigarette smoke extract （CSE） in this study. The level of nitrite （NO₂^- ）, the end metabolite of NO, activity of lactatec dehydrogenate （LDH） were measured. The activity of nitric oxide synthase （NOS ） and the L-Arginine （L-Arg） transport of lung tissue slices were also measured using the method of radiolabeled L-Arg. When rat lung tissue slices stimulated by 10% CSE, the NO₂^- release and LDH leakage increased in a time-dependent manner, both were highly related with each other （r=0.65, p<0.01 ）. The activity of NOS exhibit a significant increase induced by 10% CSE, and the rate of iNOS /cNOS was increased. 10% CSE promoted the L-Arg transport, thereby increased the maximal transport velocity （Vmax ）. 10% CSE may elevate the activity of iNOS, and supply adequate substrate for the production of NO by elevating the transport of L-Arg. Cigarette smoking may stimulates injury the lung tissue by overproducing of NO.更多还原