Article(id=1199335054599094415, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1199335049175859209, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.1606.2023.0626, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1658851200000, receivedDateStr=2022-07-27, revisedDate=null, revisedDateStr=null, acceptedDate=1664985600000, acceptedDateStr=2022-10-06, onlineDate=1763873359583, onlineDateStr=2025-11-23, pubDate=1711555200000, pubDateStr=2024-03-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1763873359583, onlineIssueDateStr=2025-11-23, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1763873359583, creator=13701087609, updateTime=1763873359583, updator=13701087609, issue=Issue{id=1199335049175859209, tenantId=1146029695717560320, journalId=1189873630562394117, year='2024', volume='49', issue='3', pageStart='245', pageEnd='366', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1763873358291, creator=13701087609, updateTime=1763874044185, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1199337926086721596, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1199335049175859209, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1199337926086721597, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1199335049175859209, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=323, endPage=328, ext={EN=ArticleExt(id=1199335055945466018, articleId=1199335054599094415, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Effect and mechanism of radiation combined with different decompression loads on acute injury of rat, columnId=1190310110212751762, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Basic Research, runingTitle=null, highlight=null, articleAbstract=

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.

, correspAuthors=Ying He, Wen-Hui Wu, authorNote=null, correspAuthorsNote=
He Ying, E-mail:
Wu Wen-Hui, E-mail:
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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。

, correspAuthors=何颖, 吴文惠, authorNote=null, correspAuthorsNote=
何颖,E-mail:
吴文惠,E-mail:
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刘敏,硕士研究生,主要从事复合伤分子机制方面的研究

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刘敏,硕士研究生,主要从事复合伤分子机制方面的研究

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刘敏,硕士研究生,主要从事复合伤分子机制方面的研究

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W/D. 湿干重比;与空白对照组比较,(1)P<0.05;与单纯辐射组比较,(2)P<0.05;与3 h比较,(3)P<0.05

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IL. 白细胞介素;TNF-α. 肿瘤坏死因子-α;与空白对照组比较,(1)P<0.05;与单纯辐射组比较,(2)P<0.05;与辐射+低负荷减压组比较,(3)P<0.05;与辐射+中负荷减压组比较,(4)P<0.05;与3 h比较,(5)P<0.05

, figureFileSmall=KnnUZSaj0984jNXgFLZxYw==, figureFileBig=sOl9+3s09TfmQmnCkGjJuA==, tableContent=null), ArticleFig(id=1199335063579099636, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1199335054599094415, language=EN, label=Fig.4, caption=Changes of the serum SOD activity and MDA content after ionizing radiation and decompression exposure in each group of rats (n=9), figureFileSmall=fEA/AaNVPlEeXVnRVFEbbQ==, figureFileBig=YXRqT8NrqGIUeJsDuq4Q3Q==, tableContent=null), ArticleFig(id=1199335063646208503, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1199335054599094415, language=CN, label=图4, caption=辐射照射后快速上浮脱险的各组大鼠血清SOD活性和MDA含量变化(n=9)

SOD. 超氧化物歧化酶;MDA. 丙二醛;与空白对照组比较,(1)P<0.05;与单纯辐射组比较,(2)P<0.05;与辐射+低负荷减压组比较,(3)P<0.05;与辐射+中负荷减压组比较,(4)P<0.05;与3 h比较,(5)P<0.05

, figureFileSmall=fEA/AaNVPlEeXVnRVFEbbQ==, figureFileBig=YXRqT8NrqGIUeJsDuq4Q3Q==, tableContent=null), ArticleFig(id=1199335063725900280, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1199335054599094415, language=EN, label=Fig.5, caption=Changes of the serum levels of NO, ICAM-1, and TXB2 after ionizing radiation and decompression exposure in each group of rats (n=9), figureFileSmall=3M+1cpAMm3LOy+GNNNbLVA==, figureFileBig=zu/rZZ953z79LVoZj8Y/sw==, tableContent=null), ArticleFig(id=1199335064845779449, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1199335054599094415, language=CN, label=图5, caption=辐射照射后快速上浮脱险的各组大鼠血清NO、ICAM-1、TXB2水平变化(n=9)

NO. 一氧化氮;ICAM-1. 细胞间黏附分子1;TXB2. 血栓素B2;与空白对照组比较,(1)P<0.05;与单纯辐射组比较,(2)P<0.05;与辐射+低负荷减压组比较,(3)P<0.05;与辐射+中负荷减压组比较,(4)P<0.05;与3 h比较,(5)P<0.05

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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
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刘敏 1, 2 , 刘光盛 2 , 王杨凯 2 , 陈锐勇 2 , 何颖 2, * , 吴文惠 1, *
解放军医学杂志 | 基础研究 2024,49(3): 323-328
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解放军医学杂志 | 基础研究 2024, 49(3): 323-328
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
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刘敏1, 2, 刘光盛2, 王杨凯2, 陈锐勇2, 何颖2, * , 吴文惠1, *
作者信息
  • 1上海海洋大学食品学院,上海 201306
  • 2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
  • 刘敏,硕士研究生,主要从事复合伤分子机制方面的研究

通讯作者:

何颖,E-mail:
吴文惠,E-mail:
Effect and mechanism of radiation combined with different decompression loads on acute injury of rat
Min Liu1, 2, Guang-Sheng Liu2, Yang-Kai Wang2, Rui-Yong Chen2, Ying He2, * , Wen-Hui Wu1, *
Affiliations
  • 1College of Food Science and Technology, Shanghai Ocean University, Shanghai 201306, China
  • 2Laboratory of Marine Biomedicine and Polar Medicine, Naval Medical Center, Shanghai 200433, China
出版时间: 2024-03-28 doi: 10.11855/j.issn.0577-7402.1606.2023.0626
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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。

辐射损伤  /  减压病  /  复合伤  /  大鼠  /  效应

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 injury  /  decompression sickness  /  combined injury  /  rat  /  effect
刘敏, 刘光盛, 王杨凯, 陈锐勇, 何颖, 吴文惠. 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. 解放军医学杂志, 2024 , 49 (3) : 323 -328 . DOI: 10.11855/j.issn.0577-7402.1606.2023.0626
Min Liu, Guang-Sheng Liu, Yang-Kai Wang, Rui-Yong Chen, Ying He, Wen-Hui Wu. Effect and mechanism of radiation combined with different decompression loads on acute injury of rat[J]. Medical Journal of Chinese People’s Liberation Army, 2024 , 49 (3) : 323 -328 . DOI: 10.11855/j.issn.0577-7402.1606.2023.0626
艇员快速上浮脱险已在各国潜艇水下事故中广泛应用,具有脱险深度大、操作简单等优点[1-3]。但艇员快速上浮时,由于短时间内压力变化较大,易发生减压病(decompression sickness,DCS)[4]。DCS是由减压性气泡引起的全身性病理生理过程,会对机体产生一定损害,严重时可致死亡[5-6] ,是危及幸存艇员脱险后健康与安全的主要医学问题。潜艇事故常伴随放射性污染,艇员在受到一定剂量辐射照射时,是否会加重DCS的发生发展,是否存在一定的时间-剂量效应,鲜有研究报道;不同损伤的复合效应也可能影响后续的伤员救治。DCS发病过程中,肺是重要靶点,主要体现在肺组织炎症反应、氧化损伤和血管内皮损伤等[7-9]。本课题组前期研究初步确定将4 Gy作为辐射复合减压损伤研究的辐照剂量。本研究通过建立大鼠模型,观察4 Gy辐射剂量暴露后不同减压负荷所致大鼠DCS发生和机体损伤的严重程度及其随时间推移的变化规律,初步探讨辐射损伤对快速上浮脱险安全性的影响及相关机制,旨在为未来脱险艇员救援与伤员救治提供实验依据。
快速上浮脱险训练舱购自烟台宏远公司;低温高速离心机购自德国 Eppendorf 公司;电子天平购自上海奔普公司;大鼠血清白细胞介素(interleukin,IL)-1β、IL-6、肿瘤坏死因子(tumor necrosis factor,TNF)-α酶联免疫检测(enzyme linked immunosorbent assay,ELISA)试剂盒购自上海基尔顿生物科技有限公司;大鼠血清超氧化物歧化酶(superoxide dismutase,SOD)、丙二醛(malondi-aldehyde,MDA)含量检测试剂盒购自南京建成生物工程研究所;大鼠血清一氧化氮(nitric oxide,NO)、细胞间黏附分子1(intercellular adhesion molecule 1,ICAM-1)和血栓素B2(thromboxane B2,TXB2)含量检测试剂盒购自上海基尔顿生物科技有限公司。
健康成年雄性SD大鼠81只,体重(190±10) g,购自上海灵畅生物科技有限公司[实验动物使用许可证号:SYXK(沪)2017-0019],饲养于海军特色医学中心动物实验中心。将大鼠随机分为空白对照组9只,单纯辐射组、辐射+低负荷减压组、辐射+中负荷减压组、辐射+高负荷减压组各18只。辐射照射剂量为4 Gy,低、中、高减压负荷分别模拟水下57 m停留30 min、45 min和60 min。大鼠适应性饲养1周后,再进行实验。本研究经海军特色医学中心动物伦理学委员会批准(NMC-2021010)。
采用海军军医大学海医系辐射中心的60Co γ射线一次性全身照射大鼠,辐照剂量4 Gy,辐照距离5.13 m,辐照时间560 s,剂量率2.199 mGy/min。辐照结束后取回大鼠进行高压暴露快速上浮脱险,采用海军特色医学中心水下医学实验室模拟潜艇脱险动物实验舱。由舱控计算机按该实验室前期预设的高气压暴露方案自动化程序,使用压缩空气以指数倍数增压方式(自动控制4 s压力翻倍的指数加压),分别模拟水下57 m停留30 min、45 min和60 min后,采用手动(30±5) s匀速减压到常压后出舱。实验舱内相对湿度40%~60%,温度26~30 ℃,减压结束后从舱中取出大鼠。空白对照组大鼠不进行辐射和高气压暴露,单纯辐射组不进行高气压暴露。减压结束后3 h和72 h分别用3 %戊巴比妥钠腹腔注射麻醉大鼠后,腹主动脉取血于离心管中静置30 min,3000 r/min离心15 min,离心后吸取上清,-80 ℃贮存备用,用于后续生化检测。
大鼠减压出舱后,观察0.5 h的行为学变化及DCS发病情况。DCS的评估指标包括呼吸急促、躁动不安、皮肤瘙痒、行走困难、四肢瘫痪或死亡。记录大鼠死亡情况。
分别于3 h和72 h取大鼠右上肺组织称湿重,再置于80 ℃恒温烘箱内烘干48 h后称量肺组织干重,并计算肺W/D。
分别于3 h和72 h取右肺中叶以10%多聚甲醛溶液(pH=7.2)固定,石蜡包埋、切片,HE染色后,光学显微镜下观察病理学变化。
按照试剂盒说明书步骤采用ELISA法测定血清中IL-1β、IL-6、TNF-α含量,测定450 nm处的吸光度(optical density,OD)值。
按照试剂盒说明书步骤采用羟胺法检测血清中SOD活性,测定550 nm处的OD值;按照试剂盒说明书步骤采用硫代巴比妥酸(thiobarbituric acid,TBA)法检测血清中MDA含量,测定532 nm处的OD值。
按照试剂盒说明书步骤采用硝酸还原酶法测定血清中NO水平,测定550 nm处的OD值。按照试剂盒说明书步骤采用ELISA法测定血清中ICAM-1和TXB2水平,测定450 nm处的OD值。
采用SPSS 26.0软件进行统计分析,GraphPad Prism 8.3.0软件制图。计数资料以例(%)表示,采用χ2检验;计量资料符合正态分布,以$\bar{x}±s$表示,组间比较采用单因素方差分析,进一步两两比较采用LSD-t检验。P<0.05为差异有统计学意义。
4 Gy辐射照射后,大鼠均表现出不同程度的疲倦态。与空白对照组(0)和单纯辐射组(0)比较,辐射+低负荷减压组大鼠伤死率[5.6%(1/18)]差异无统计学意义(P>0.05),辐射+中负荷减压组[44.4%(8/18)]和辐射+高负荷减压组大鼠伤死率[50.0%(9/18)]均明显增高(P<0.05)。与辐射+中负荷减压组比较,辐射+高负荷减压组大鼠伤死率差异无统计学意义(P>0.05)。
与空白对照组比较,减压结束后3 h各组大鼠肺W/D差异均无统计学意义(P>0.05),减压结束后72 h各组大鼠肺W/D均明显升高(P<0.05);除空白对照组外,与减压结束后3 h时比较,减压结束后72 h各组大鼠肺W/D均明显升高(P<0.05);与单纯辐射组比较,减压结束后72 h辐射+高负荷减压组大鼠肺W/D明显增高(P<0.05),其他各组大鼠肺W/D差异均无统计学意义(P>0.05,图1)。
HE染色显示,与空白对照组比较,单纯辐射组大鼠肺间质轻度水肿,肺泡壁增厚,红细胞分散分布在肺间质,肺泡腔未见红细胞渗出;辐射+低负荷减压组(3 h)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、充血以及炎性细胞浸润的病理特征更为严重。与减压结束后3 h比较,减压结束后72 h各组大鼠肺病理表现未见改善(图2)。
与空白对照组比较,其他各组大鼠血清IL-1β、IL-6、TNF-α水平均明显升高(P<0.05);与单纯辐射组比较,各辐射+减压组大鼠血清IL-1β、IL-6、TNF-α水平均明显升高(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IL-1β、IL-6水平均明显升高(P<0.05)。除空白对照组外,与减压结束后3 h比较,各组减压结束后72 h血清IL-1β、IL-6、TNF-α水平均明显降低(P<0.05,图3)。
与空白对照组和单纯辐射组比较,各辐射+减压组血清SOD活性均明显降低(P<0.05),MDA含量均明显增高(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SOD活性均明显降低(P<0.05),MDA含量均明显增高(P<0.05)。除空白对照组外,与减压结束后3 h取材时比较,各组减压结束后72 h取材时血清SOD活性均明显增强(P<0.05),MDA含量均明显降低(P<0.05,图4)。
与空白对照组和单纯辐射组比较,各辐射+减压组大鼠血清NO、ICAM-1、TXB2水平均明显增高(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ICAM-1、TXB2水平均明显增高(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NO、ICAM-1、TXB2水平均明显降低(P<0.05,图5)。
幸存艇员从水下失事潜艇实施逃生需要经历高气压暴露。虽然快速上浮脱险在技术上按照不减压潜水原则实施,但一旦深度增加或潜艇固壳破损致艇员有一定压强的暴露后,减压负荷是可能危及脱险艇员生命和健康的首要问题[10-12]。潜艇水下事故伴随辐射暴露时,幸存艇员一般需要尽快实施上浮脱险,评估辐射照射后实施潜艇脱险的DCS发病概率是相关救援研究的重要内容,其中辐射与减压损伤的复合效应受到关注。本研究结果显示,单纯4 Gy辐照的大鼠未出现死亡,而辐射+减压组大鼠均出现死亡;大鼠死亡均发生在减压处理后即刻。逃生的潜艇艇员往往需要在逃生到水面后待援。本研究中大鼠减压结束后72 h的病理生理状态可一定程度反映上浮脱险后海面待援的幸存复合伤艇员状态。本研究动物模型的减压负荷体现在最大压强下暴露时间的长短,后者直接决定机体组织的惰性气体饱和量,即减压过程需要脱离机体组织溶解的量。本研究结果显示,随着减压负荷增加,辐射+减压复合损伤大鼠的伤死率明显增高,提示类似的潜艇事故后,幸存艇员应尽快实施脱险。
肺是减压损伤的主要靶器官。高气压暴露后的减压过程中,机体组织惰性气体脱饱和形成的气泡主要存在于静脉系统,并随着血液流动汇聚到右心,经肺动脉阻拦在肺毛细血管网中[13]。肺W/D能较好地反映肺微血管通透性和肺组织水肿程度[14]。肺毛细血管中的气泡可引起血管屏障的损伤反应,导致其通透性改变,蛋白和白细胞即可进入血管周围组织,从而引起肺间质增厚、肺组织水肿充血,甚至肺泡内渗出等病理表现[715-16]。本研究结果显示,辐射照射+减压损伤可诱导肺微血管损伤,这或许是复合损伤效应发生的病理基础;然而,复合致伤组3 h取材的大鼠肺W/D与空白对照组差异显著,但与单纯辐射组差异不显著;72 h取材的辐射+高负荷减压组与更小减压负荷组差异不显著,但与单纯辐射组差异显著,提示辐照+减压的复合损伤效应随着致伤后时间延长有所加重,肺组织病理结果也验证了这一变化。提示,在黄金72 h救援时间内,辐照+减压的复合损伤会加重脱险的幸存艇员肺病理进程,援潜救生时应重视这一点。
在快速上浮脱险致DCS的过程中诱导循环气泡可能会对组织施加压力,影响血管腔表面活性剂层和内皮细胞的激活,导致血小板和白细胞聚集、细胞因子释放、补体激活和凝血级联反应[8-9]。研究显示,高压暴露可促进氧化应激[7]。此外,NO作为一种较强的血管扩张剂,有助于维持血管内稳态。研究显示,NO释放剂可减少气泡形成,预防严重的DCS[17]。NO、TXB2是内皮细胞分泌的血管活性物质,ICAM-1是能够反映内皮损伤的敏感生物标志物。辐射通过诱导自由基和 DNA 损伤,促进放射性肺炎期间出现的氧化应激、血管损伤和炎症[18-20]。持续性炎症维持肺泡上皮和血管内皮细胞损伤,并导致病理变化,包括免疫细胞浸润、毛细血管通透性增加和肺水肿[21-23]。TNF-α是由活化的巨噬细胞产生的促炎细胞因子,其可刺激成纤维细胞生长和胶原酶产生,并激活其他促炎细胞因子(IL-1、IL-6和IFN-γ)的级联反应[24]。早期释放TNF-α是肺部受照射后的一个关键因素[25-26]。IL-1β、TNF-α和其他细胞因子可激活诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS),进而产生大量NO[27]。本研究对炎性因子、氧化应激指标、血管损伤标志物的检测结果显示,单纯辐射组和各辐射+减压组大鼠血清IL-1β、IL-6、TNF-α、MDA、NO、ICAM-1和TXB2含量均明显增加,SOD活性明显降低;与单纯辐射组比较,各辐射+减压组大鼠血清IL-1β、IL-6、TNF-α、MDA、NO、ICAM-1和TXB2含量均明显增加,SOD活性明显降低,且随着减压负荷增加,IL-1β、IL-6、TNF-α、MDA、NO、ICAM-1和TXB2含量均增加,SOD活性降低;同组别不同时间点比较,减压结束后72 h损伤指标含量相较于3 h均明显下降。表明固定辐射剂量(4 Gy)下,随着减压负荷增加,大鼠血清IL-1β、IL-6、TNF-α等含量均明显增高,炎症反应加剧,提示早期抗感染、抗炎等措施应得到重视;氧化应激SOD活性随着减压负荷的增加明显降低,MDA水平随着减压负荷的增加明显增高,提示辐射和减压损伤在氧化-抗氧化水平上存在复合效应;血管舒缩因子NO、凝血因子TXB2和ICAM-1水平随着减压负荷增加明显增高,提示辐射和减压损伤可导致血液高凝血状态,其复合损伤效应的潜在机制与炎症、免疫应激、氧化损伤、血管舒缩活性和凝血机制相关。
本研究的局限主要在于:(1)基于目前的实验结果还无法明确得出随着时间推移,机体损伤是否存在自我修复与适应,需通过设置更多时间节点来进行观察;(2)辐射和减压损伤复合效应的相关机制尚待进一步探讨。
综上所述,本研究结果显示,高减压负荷可致辐照+高气压暴露后大鼠伤死率增高,提示失事潜艇并发放射性污染时艇员应尽快实施脱险;辐射和减压损伤复合效应的潜在机制与炎症、免疫应激、氧化损伤、血管舒缩活性及凝血机制等相关,应在相关伤员救治中予以关注。
  • 军队后勤科研重点项目(BHJ16J021)
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doi: 10.11855/j.issn.0577-7402.1606.2023.0626
  • 接收时间:2022-07-27
  • 首发时间:2025-11-23
  • 出版时间:2024-03-28
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  • 收稿日期:2022-07-27
  • 录用日期:2022-10-06
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Logistics Research Project of PLA(BHJ16J021)
军队后勤科研重点项目(BHJ16J021)
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    1上海海洋大学食品学院,上海 201306
    2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

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2种不同金属材料的力学参数

Family
属数
Number of
genus
种数
Number of
species
占总种数比例
Percentage of
total species (%)

Genus
种数
Number of
species
占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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