首页|辐射复合不同减压负荷暴露致大鼠急性损伤的效应及其可能的机制

辐射复合不同减压负荷暴露致大鼠急性损伤的效应及其可能的机制

扫码查看
目的 观察特定辐射剂量复合减压暴露致大鼠损伤的效应及其可能的机制。方法 81只雄性SD大鼠,随机分为空白对照组(n=9)、单纯辐射组(n=18)、辐射+低负荷减压组(n=18)、辐射+中负荷减压组(n=18)和辐射+高负荷减压组(n=18)。除空白对照组外,大鼠接受4 Gy的60Co γ射线全身照射,然后进行快速上浮脱险实验,高气压暴露方案分别为在水下57 m停留30 min、45 min或60 min后(30±5)s内减至常压,单纯辐射组不进行高气压暴露。出舱后0。5 h观察各组大鼠行为和死亡情况,分别于3 h和72 h取血(腹主动脉)和肺组织,分析肺湿/干重比(W/D)、肺组织病理及血清白细胞介素(IL)-1β、IL-6、肿瘤坏死因子-α(TNF-α)、超氧化物歧化酶(SOD)、丙二醛(MDA)、一氧化氮(NO)、细胞间黏附分子1(ICAM-1)和血栓素B2(TXB2)含量的变化。结果 与空白对照组和单纯辐射组比较,辐射+低负荷减压组大鼠伤死率差异无统计学意义(P>0。05),辐射+中负荷减压组和辐射+高负荷减压组大鼠伤死率均明显增高(P<0。05)。与空白对照组比较,其他各组大鼠减压结束后3 h肺W/D差异均无统计学意义(P>0。05),减压结束后72 h肺W/D均升高(P<0。05)。HE染色结果显示,与空白对照组比较,单纯辐射组大鼠肺间质轻度水肿;辐射+低负荷减压组大鼠肺组织水肿明显,肺泡腔内可见少量红细胞渗出;辐射+中负荷减压组和辐射+高负荷减压组大鼠肺组织水肿、充血及炎性细胞浸润更为严重。与空白对照组和单纯辐射组比较,各辐射+减压组血清IL-1β、IL-6、TNF-α、MDA、NO、ICAM-1、TXB2水平均升高(P<0。05),SOD活性均降低(P<0。05);与辐射+低负荷减压组比较,辐射+中负荷减压组和辐射+高负荷减压组大鼠血清IL-1β、IL-6、MDA、ICAM-1、TXB2水平均增高(P<0。05),SOD活性均降低(P<0。05);除空白对照组外,与减压结束后3 h比较,各组大鼠减压结束后 72 h血清IL-1β、IL-6、TNF-α、MDA、NO、ICAM-1、TXB2 水平均降低(P<0。05),SOD活性均增强(P<0。05)。结论 高减压负荷可致辐照+高气压暴露的大鼠伤死率增高,辐射和减压复合损伤效应的潜在机制可能与炎症、免疫应激、氧化损伤、血管舒缩活性和凝血机制相关。
Effect and mechanism of radiation combined with different decompression loads on acute injury of rat
Objective To investigate the effect of rats'injuries and its mechanism caused by specific dose of radiation combined with decompression exposure.Methods 81 male SD rats were randomly divided into control group(n=9),radiation group(n=18),radiation+low-load decompression group(n=18),radiation+medium-load decompression group(n=18),and radiation+high-load decompression group(n=18).In addition to control group,the rats were irradiated with 60Co γ rays at 4 Gy and then underwent rapid escape experiments.The high-pressure exposure schemes were to stay underwater 57 m for 30 min,45 min or 60 min and reduce to normal pressure within(30±5)s,respectively.The high-pressure exposure was not carried out in radiation group.The behavior and death of rats in each group were observed 0.5 h after leaving the cabin.Blood(abdominal aorta)and lung tissues were collected at 3 h and 72 h,respectively.The changes of lung wet-dry weight ratio(W/D),lung pathology and serum levels of interleukin(IL)-1β,IL-6,tumor necrosis factor-α(TNF-α),superoxide dismutase(SOD),malondialdehyde(MDA),nitric oxide(NO),intercellular adhesion molecule-1(ICAM-1)and thromboxane B2(TXB2)were analyzed.Results Compared with control group and radiation group,radiation+low-load decompression group showed no significant difference in the injury and death rate of rats(P>0.05),while radiation+medium-load decompression group and radiation+high-load decompression group showed significantly increase of the injury and death rate of rats(P<0.05).Compared with control group,other groups showed no significant change in pulmonary W/D at 3 h(P>0.05),and increased at 72 h(P<0.05).HE staining showed that compared with control group,radiation group showed mild lung interstitial edema,while radiation+low-load decompression group showed obvious pulmonary tissue edema and a small number of red blood cells exudated in the alveolar cavity.The edema,congestion and inflammatory cell infiltration of lung tissue were more serious in radiation+medium-load decompression group and radiation+high-load decompression group.Compared with control group and radiation group,all radiation+decompression groups showed an increase in serum levels of IL-1β,IL-6,TNF-α,MDA,NO,ICAM-1 and TXB2(P<0.05),and a decrease in SOD activity(P<0.05).Compared with radiation+low-load decompression group,radiation+medium-load decompression group and radiation+high-load decompression group showed increase in serum levels of IL-1β,IL-6,MDA,ICAM-1 and TXB2(P<0.05),and decrease in activity of SOD(P<0.05).Except for control group,serum levels of IL-1β,IL-6,TNF-α,MDA,NO,ICAM-1 and TXB2 were decreased at 72 h compared with 3 h(P<0.05),and SOD activity was increased at 72 h in all groups(P<0.05).Conclusions High-load decompression can increase the injury and death rate of rats exposed to radiation and high pressure.The potential mechanism of the combined injury effect of radiation and decompression was related to inflammation,immune stress,oxidative damage,vasomotor activity and coagulation mechanism.

radiation injurydecompression sicknesscombined injuryrateffect

刘敏、刘光盛、王杨凯、陈锐勇、何颖、吴文惠

展开 >

上海海洋大学食品学院,上海 201306

海军特色医学中心海洋生物医药与极地医学研究室,上海 200433

辐射损伤 减压病 复合伤 大鼠 效应

军队后勤科研重点项目

BHJ16J021

2024

解放军医学杂志
人民军医出版社

解放军医学杂志

CSTPCD北大核心
影响因子:1.644
ISSN:0577-7402
年,卷(期):2024.49(3)
  • 27