辐射合并减压暴露致大鼠急性肺损伤的效应观察

Effects of radiation combined with decompression exposure on acute lung injury in rats

  • 摘要:
    目的 探讨不同剂量辐射暴露对快速上浮脱险致大鼠减压病急性肺损伤及死亡率的影响。
    方法 53只SD大鼠按体重分层后以随机数表法分为5组:空白对照组(10只)、单纯减压组(10只)、4 Gy照射+减压组(11只)、6 Gy照射+减压组(11只)以及8 Gy照射+减压组(11只)。照射组大鼠先进行4、6、8 Gy不同剂量60Co γ射线全身照射,空白对照组及单纯减压组大鼠在相同环境下不进行照射;照射结束后1 h各减压组再进行减压处理实验(57 m停留45 min后,37 s快速减压至大气压),观察各组大鼠死亡率、肺湿干重比、肺组织病理损伤程度以及肺泡灌洗液中炎症因子和氧化应激相关分子水平的变化。各组大鼠死亡率的比较采用卡方检验,其他指标的比较采用单因素方差分析,进一步两两比较采用LSD-t检验。
    结果 与空白对照组比较,各实验组大鼠死亡数量和肺湿干重比均增加,6 Gy照射+减压组和8 Gy照射+减压组大鼠肺湿干重比显著增加,且差异有统计学意义(F=3.096,LSD-t=2.758、2.959;均P<0.05);各实验组大鼠肺组织病理损伤明显,其中6 Gy照射+减压组和8 Gy照射+减压组更为显著;各实验组大鼠肺泡灌洗液中白细胞介素1β(IL-1β)、白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)和丙二醛(MDA)水平显著增加,且差异有统计学意义(F=45.680~78.270,均P<0.01),超氧化物歧化酶(SOD)活力和谷胱甘肽过氧化物酶(GSH-Px)水平显著下降,且差异有统计学意义(F=35.720、51.370,均P<0.01)。与单纯减压组比较,4 Gy照射+减压组和8 Gy照射+减压组大鼠死亡数量增加,但死亡率的差异无统计学意义(χ2=7.925,P>0.05);各照射组大鼠肺湿干重比虽有上升趋势,但差异无统计学意义(LSD-t=0.901、1.818、2.020,均P>0.05);各照射组大鼠肺组织病理损伤有不同程度的加重,其中8 Gy照射+减压组损伤程度最重;各照射组大鼠肺泡灌洗液中炎症因子(IL-1β、IL-6、TNF-α)和氧化应激相关分子(SOD、GSH-Px、MDA)均变化显著(LSD-t=3.081~8.265,均P<0.01),其中6 Gy照射+减压组变化最为显著。
    结论 辐射会加重快速上浮脱险造成的肺组织炎症和氧化应激损伤,表现为肺组织病理损伤程度加重及死亡率增加,从而增加快速上浮脱险致减压病发生的风险。

     

    Abstract:
    Objective To investigate the effects of different doses of radiation exposure on acute lung injury and mortality from decompression sickness (DCS) induced by rapid floating escape in rats.
    Methods A total of 53 Sprague-Dawley rats were stratified in accordance with body weight and divided into 5 groups by using a random number table method. The groups were as follows: blank control group (10 rats), simple decompression group (10 rats), 4 Gy irradiation with decompression group (11 rats), 6 Gy irradiation with decompression group (11 rats), and 8 Gy irradiation with decompression group (11 rats). The animals in the irradiation groups were given different doses of 60Co γ whole-body radiation and then exposed to decompression treatment (i.e., after staying at a depth of 57 m for 45 min, the rats were made to ascend quickly to atmospheric pressure within 37 s) 1 h after irradiation. The mortality rate, lung wet-dry weight ratio, degree of lung tissue pathological damage, and changes in levels of inflammatory factors and oxidative stress-related molecules in the alveolar lavage fluid were observed in each group of rats. Mortality rates among groups were compared using Chi-square test, while the remaining variables were analyzed using one-way ANOVA. Further comparison between two groups using LSD t-test.
    Results Compared with that in the blank control group, the number of animal deaths and the lung wet-dry weight ratio increased in each experimental group, with the lung wet-dry weight ratio increasing significantly in the 6 Gy and 8 Gy irradiation with decompression groups (F=3.096, LSD-t=2.758, 2.959; all P<0.05). The pathological damage of lung tissues in each experimental group was evident, and those in the 6 Gy and 8 Gy irradiation with decompression groups were more significant among the irradiation groups. The interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and malondialdehyde (MDA) in the bronchoalveolar lavage fluid of each experimental group were significantly increased (F=45.680–78.270, all P<0.01), whereas superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were significantly decreased (F=35.720, 51.370; both P<0.01). Compared with that in the simple decompression group, the number of animal deaths in the 4 Gy and 8 Gy irradiation with decompression groups increased, but no statistical difference was noted in the mortality rate (χ2=7.925, P>0.05). Although the lung wet-dry weight ratio of the rats in each irradiation group exhibited an upward trend, no statistically significant difference was found (LSD-t=0.901, 1.818, 2.020; all P>0.05). The pathological damage of lung tissues was aggravated to different degrees, and the damage degree of the 8 Gy irradiation with decompression group was the most serious. Inflammatory factors (IL-1β, IL-6, and TNF-α) and oxidative stress-related molecules (SOD, GSH-Px, and MDA) in bronchoalveolar lavage fluid changed significantly (LSD-t=3.081–8.265, all P<0.01). Among which, the 6 Gy irradiation with decompression group exhibited the most significant change.
    Conclusions Nuclear radiation can worsen lung tissue inflammation and oxidative stress damage caused by rapid floating escape. Such effect is manifested as aggravated lung tissue pathological damage and increased mortality, increasing the risk of DCS caused by rapid floating escape.

     

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