载气吹扫尼古丁长期吸入对大鼠心血管功能、氧化应激和炎症水平影响

目的 研究载气吹扫尼古丁吸入对大鼠心血管功能、氧化应激和炎症水平的影响并初步探讨其机制.方法 将40只雄性健康SD大鼠随机均分为4组.实验组进行载气吹扫尼古丁法致大鼠吸入,每日分别定时暴露1、2、4 h,确定为低、中、高剂量组.对照组在标准条件下饲养. 90 d后,测定大鼠心功能,心、肺、血清中内皮型一氧化氮合酶( eNOS)、白介素1β(IL-1β)、肿瘤坏死因子α(TNF-α)、白介素10(IL-10)含量,血清中超氧化物歧化酶( SOD)活性和丙二醛(MDA)含量.结果 与对照组比较,暴露处理组血压明显 升高,血清SOD活性降低,谷胱甘肽过氧化物酶( GSH-Px)含量升高,而 MDA含量明显降低.心、肺血清 IL-1β、TNF-α、IL-10 含量均有不同程度的升高.结论 载气吹扫尼古丁吸入的大鼠血压升高,心功能存在障碍,机体氧化-抗氧化失衡并且心肺发生炎症反应,其机制可能与内皮细胞功能紊乱和交感、副交感系统的同时激活有关.

Effects of long-term inhalation of nicotine by gas-purge on cardiovascular function,oxidative stress and inflammation in rats

Objective To investigate the effects of inhalation of nicotine on cardiovascular function, oxidative stress and inflammation in rats and its mechanism. Methods Forty healthy male SD rats were randomly divided into four groups. The experimental group was inhaled nicotine by air-purging. The rats were exposed for 1 h, 2 h and 4 h daily, respectively, and were determined as low, medium and high dose groups. The control group was housed un-der standard conditions. After 90 days, aortic reactivity and blood pressure were measured. The levels of endotheli-al NO synthase(eNOS), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) in heart, lung tissue and serum of rats were measured. Serum nitric oxide ( NO ) content, malondialdehyde ( MDA) content, superoxide dismutase ( SOD) activity and glutathione peroxidase ( GSH-Px) activity were meas-ured respectively. Results Compared with the control group, the blood pressure of the experimental group was sig-nificantly increased. NO, eNOS and MDA content were significantly decreased. GSH-Px activity was significantly increased. The levels of IL-1β, TNF-α, IL-10 were significantly increased in heart, lung and serum respectively. Conclusion Long-term inhaled nicotine by air-purged impaired cardiac function and caused high blood pressure, induced oxidative stress and cardiopulmonary inflammatory reaction. The mechanism may be related to endothelial dysfunction and simultaneous activation of sympathetic and parasympathetic systems.