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目的本研究探讨长期胺碘酮不同剂量对大鼠肺脏的影响。方法随机选择雄性SD大鼠30只,随机分为对照组(NC,n=10),胺碘酮低剂量组[n=10,50 mg/(kg·d),AM50],胺碘酮高剂量组[n=10,200 mg/(kg·d),AM200],每天上午给药1次,对照组喂等量的自来水,连续15周。期间观察SD大鼠一般状况、体重,15周后麻醉后股动脉抽血测PⅢNP(Ⅲ型前胶原N端肽)、Ⅳ-Col(Ⅳ型胶原)水平,处死后称取肺脏重量,计算脏器系数,并进行病理组织检查。结果 AM200组体重增长慢于其他2组,从第2周起与其他2组比较差异均存在统计学意义(P<0.05),累积死亡3只,其余2组未见死亡;肺脏重量[NC(1.58±0.17)g;AM50(1.54±0.16)g;AM200(1.57±0.55)g]及脏器系数(NC 0.32±0.04;AM50 0.30±0.03;AM200 0.38±0.13),3组之间肺脏重量及脏器系数差异均无统计学意义(P>0.05);3组PⅢNP水平取Ln10后[NC(0.60±0.40)μg/L;AM50(0.36±0.26)μg/L;AM200(0.79±0.59)μg/L],Ⅳ-Col水平[NC(1.02±0.38)μg/L;AM50(0.81±0.23)μg/L;AM200(1.21±1.00)μg/L],3组PⅢNP、Ⅳ-Col水平差异未见统计学意义(P>0.05);病理检查AM50组可见泡沫细胞,AM200组可见有若干炎性坏死灶,伴轻度纤维化,有多个多核巨细胞,支气管、细支气管上皮节段空泡变性,肺泡腔内有大量巨噬细胞、脱落的上皮细胞及渗出液。电镜可见AM50组Ⅱ型肺上皮细胞板层体空泡,AM100组可见板层电体空泡,绒毛清晰。结论胺碘酮通过诱发炎症反应导致细胞损伤坏死,最终导致肺纤维化。
Objective This study was to investigate the effects of different doses of long-term amiodarone on rat lungs. Methods Thirty male SD rats were randomly divided into control group (NC, n = 10), amiodarone low dose group (n = 10,50 mg / (kg · d), AM50], amiodarone high The dose group [n = 10,200 mg / (kg · d), AM200] was given once a day in the morning and the control group fed the same amount of tap water for 15 weeks. The general condition and body weight of SD rats were observed. The level of PⅢNP (type Ⅲ procollagen N-terminal peptide) and Ⅳ-Col (type Ⅳ collagen) in the femoral artery after anesthesia were measured 15 weeks later. Coefficients, and pathological examination. Results The body weight of AM200 group was slower than that of the other two groups. The difference between the two groups was statistically significant (P <0.05) from the second week to the end of the third week. There were three cumulative deaths and no deaths in the other two groups. The lung weight [NC ( 1.58 ± 0.17) g; AM50 (1.54 ± 0.16) g; AM200 (1.57 ± 0.55) g] and organ coefficient (NC 0.32 ± 0.04; AM50 0.30 ± 0.03; AM200 0.38 ± 0.13) (P> 0.05). The levels of PⅢNP in the three groups were significantly higher than those in the control group (P <0.05) / L], the level of IV-Col was significantly higher in the three groups (NC (1.02 ± 0.38) μg / L, AM50 (0.81 ± 0.23) μg / L and AM200 See statistical significance (P> 0.05). Pathological examination showed that the foam cells were found in the AM50 group. There were some inflammatory necrosis lesions in the AM200 group with mild fibrosis, multiple multinucleated giant cells, bronchial and bronchial epithelial segmental vacuoles Degeneration, a large number of alveolar macrophages, shedding of epithelial cells and exudate. Electron microscopy showed AM50 group Ⅱ type lung epithelial cells lamellar vacuoles, AM100 group visible lamellar electrical cavities, villi clear. Conclusions Amiodarone induces cell injury and necrosis by inducing inflammatory reaction, which eventually leads to pulmonary fibrosis.