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气管损伤

气管损伤的相关文献在1992年到2020年内共计65篇,主要集中在外科学、耳鼻咽喉科学、临床医学 等领域,其中期刊论文61篇、会议论文4篇、相关期刊50种,包括泰州职业技术学院学报、工企医刊、齐鲁护理杂志等; 相关会议4种,包括第五届全军器官移植学术会议、全国医院病案管理、统计工作新进展(重庆)学术研讨会、《中华急诊医学杂志》第七届组稿会等;气管损伤的相关文献由167位作者贡献,包括孔令文、孙丽华、孙姝等。

气管损伤—发文量

期刊论文>

论文:61 占比:93.85%

会议论文>

论文:4 占比:6.15%

总计:65篇

气管损伤—发文趋势图

气管损伤

-研究学者

  • 孔令文
  • 孙丽华
  • 孙姝
  • 孟晓
  • 季鹏
  • 宋卜
  • 张广忖
  • 徐睿
  • 曾丁
  • 王涛
  • 期刊论文
  • 会议论文

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    • 徐明鹏; 李莉华; 甘罗曼; 柳广南; 甘敬华; 覃恩愿; 孟晓燕; 肖阳宝
    • 《国际呼吸杂志》  | 2017年
    • 摘要: Objective To explore the mechanism of prevention effect of erythromycin on tracheal stenosis in tracheal injury rabbit models.Methods Eighteen rabbits were randomly divided into three groups.The trachea were directly closed after tracheotomy in negative control group,the tracheal mucosa was scraped by a nylon brush after tracheotomy in model control group and erythromycin treated group.On the seventh day before operation,the rabbits in erythromycin treated group received intragastric administration of 13.6 mg/kg erythromycin daily until the tenth day after operation,the rabbits in negative control group and model control group received equivalent saline daily.Pathological changes and the degree of stenosis were assessed by hematoxylin and eosin staining,transforming growth factor-β1 (TGF-β1) mRNA expression was determined by real-time polymerase chain reaction,and the expressions of type Ⅰ collagen and type Ⅲ collagen were detected by immunohistochemistry.Results The tracheal stenosis rate was respectively (35.11 ± 4.50)%,(11.96 ± 3.26)%,and (53.95 ± 7.09)% in erythromycin treated group,negative control group,and model control group.The tracheal stenosis rate in erythromycin treated group was lower than that in model control group (t =13.98,P <0.05).Pathology result showed more inflammatory cell infiltration,fibroblast proliferation,and a large number of small angiogenesis in model control group,but these features were reduced in erythromycin treated group.The expression of TGF-β1 mRNA in erythromycin treated group was lower than that in model control group (t =4.55,P <0.05).Immunohistochemistry result showed that the expressions of type Ⅰ collagen and type Ⅲ collagen in tracheal stenosis tissue of erythromycin treated group were down-regulated compared with model control group (all P <0.05).Conclusions Erythromycin has a preventive effect on tracheal stenosis through the down-regulation of expressions of TGF-β1,type Ⅰ collagen and type Ⅲ collagen in tracheal injury rabbits.%目的 探讨红霉素在预防兔气管损伤后气管狭窄的作用及机制.方法 18只新西兰大耳白兔随机分为阴性对照组、模型对照组、红霉素治疗组,每组均行气管切开,阴性对照组气管切开后直接缝合气管,其余2组气管切开尼龙刷刮除气管黏膜后缝合气管.红霉素治疗组术前7d开始给予红霉素13.6mg/kg,每日灌胃至术后10 d,阴性对照组、模型对照组每日灌胃等量生理盐水.术后10 d处死兔子,收集气管组织,HE染色检查气管组织病理学改变并测量气管狭窄率;实时定量PCR检测各组气管组织转化生长因子β1 (TGF-β1) mRNA表达;免疫组化法检测气管组织Ⅰ型胶原蛋白、Ⅲ型胶原蛋白的表达.结果 红霉素治疗组气管狭窄率为(35.11±4.50)%,阴性对照组气管狭窄率为(11.96±3.26)%,模型对照组气管狭窄率为(53.95±7.09)%,红霉素治疗组气管狭窄率低于模型对照组(t=13.98,P<0.05).组织病理学结果显示,模型对照组气管狭窄组织中较多炎性细胞浸润,成纤维细胞大量增殖,大量小血管生成,而红霉素治疗组炎性细胞浸润、成纤维化细胞增殖、小血管生成均减少.红霉素治疗组TGF-β1 mRNA相对表达量较模型对照组减少(t=4.55,P<0.05).免疫组化结果显示,红霉素治疗组的工型胶原蛋白、Ⅲ型胶原蛋白的表达量均较模型对照组明显降低(P值均<0.05).结论 红霉素可能通过抗炎,下调TGF-β1、Ⅰ型胶原蛋白、Ⅲ型胶原蛋白表达,减轻兔气管损伤后气管狭窄.
    • 孟新科
    • 《医师在线》  | 2016年
    • 摘要: 临床上,在院前急救或院内抢救创伤的患者中,须进行呼吸道管理的多为头、颈、胸等部位损伤或多发伤的患者,如头面部损伤、开放性颅骨骨折、颅内出血、脑疝喉、气管损伤(环状、甲状、杓状软骨损伤,气管离断)、胸部损伤(肋胸骨骨折、肺挫裂伤、血气胸、张力性气胸)、
    • 祝筱姬; 徐睿; 孟晓; 季鹏; 赵超; 韩玮; 王涛; 郭文君
    • 《重庆医学》  | 2014年
    • 摘要: 目的:建立大鼠芥子气(SM )气管损伤模型,探讨SM致大鼠气管急性损伤的机制。方法雄性SD大鼠全身麻醉下气管插管,SM组(32只)气管内注入稀释SM (2.0 mg/kg ,0.1 mL ),丙二醇对照组(32只)注入丙二醇0.1 mL ,正常对照组(8只)不做任何处理。获取组织和血标本,行 HE染色、免疫组织化学、血清炎性因子及酶测定。结果 SM 组黏膜下有大量淋巴细胞浸润;上皮层和黏膜下层凋亡细胞Caspase-3和Caspase-9表达阳性;血清TNF-α、IL-1β、IL-6水平24 h达高峰;血清乳酸脱氢酶(LDH)、谷胱甘肽过氧化物酶(GP)、γ谷氨酰转移酶(GGT)、硫代巴比妥酸反应物质(TBARS)水平6 h或24 h达到高峰。丙二醇对照组与正常对照组黏膜下层淋巴细胞、巨噬细胞、中性粒细胞均少见。结论 SM (2.0 mg/kg)致大鼠气管急性损伤机制涉及炎性反应、细胞凋亡、氧化应激,且损伤程度与时间有相关性。%Objective To establish the sulfur mustard (SM ) induced tracheal injury model in rat and to investigate its mecha-nism .Methods Male rats (SD) were anesthetized and intra-tracheally intubated .The SM group was intra-tracheally injected by 2 mg/kg of diluted SM ,while the propylene glycol control group only by 0 .1mL of propylene glycol and the normal control group had no any treatment .The tissue and blood samples were taken for conducting the HE and immunohistochemical staining and measuring serum enzymes and andinflammatory factors .Results In the SM group ,a large number of lymphocytes infiltration in submucosa were observed;the positive expression of caspase-3 and caspase-9 were observed in epithelium and submucosa ;serum levels of TNF-α,IL-1β,IL-6 reached the peak in 24 h;serum levels of LDH ,GP ,BARS reached the peak in 6h ,so did GGT in 24 h .In the propyl-ene glycol control group and the normal control group ,lymphocytes ,macrophages and neutrophils were rare in submucosa .Conclu-sion The mechanism of SM (2 mg/kg) induced acute tracheal injury involves the inflammatory reaction ,apoptosis and oxidative stress ,moreover the lesion degree has the correlation with time .
    • 孟晓; 郭文君; 张圣明; 祝筱姬; 徐睿; 赵超; 连承进; 季鹏; 王涛; 鞠玲燕; 王美红
    • 《国际呼吸杂志》  | 2014年
    • 摘要: Objective To establish an animal model for rat respiratory tract injury due to sulfur mustard (SM),and observe the morphologic changes of tracheal tissues and epithelial cells in SM-induced injury.Methods Male SD rats (n =72)were randomly divided into three groups (SM group,propylene glycol group,and normal group).The rats in the SM (2 mg/kg)group were injected intratracheally with diluted SM (0.1 ml).Histomorphologic and cytomorphogic changes of the specimen were observed under light and electron microscopy.Results In the SM group,histomorphologic changes included shed tracheal epithelial cells,focal ulcer formation,deranged cilia,increased glands in the lamia propria mucosae,and inflammatory cells invading the submucosa.The cytomorphologic changes were as follows:the cellular membranes lacking,medullary changes in the mitochondria with difficult to discern mitochondrial cristae appeared in goblet cells,and difficult to discern karyotheca,karyopyknosis,and margination of the nuclear chromatin in cilia,basal cells,fibroblasts.The structure of tracheal tissue and epithelial cells of the propylene glycol group was the same as the control group.Conclusions SM (2 mg/kg)can cause acute injury of tissues and multi-epithelial cells of the rat trachea.The degree of injury is positively correlated to the duration of time.SM mainly affects the cellular membranes and organelles of goblet cells,as well as nuclear chromatin of cilia,basal cells,and fibroblasts.%目的:建立芥子气致大鼠呼吸道损伤的动物模型,观察芥子气损伤大鼠气管的组织和细胞形态学变化。方法雄性大鼠72只,随机分为芥子气组(n =32)、丙二醇对照组(n =32)和正常对照组(n =8)。芥子气组气管内注入稀释的芥子气(0.1 ml,2 mg/kg),光镜和电镜下观察气管组织和细胞形态学改变。结果芥子气组(6 h、24 h、48 h、72 h)光镜所见:气管黏膜上皮细胞部分脱落,灶性溃疡形成,纤毛紊乱,黏膜固有层腺体增多,黏膜下层大量炎细胞浸润。芥子气组(72 h)电镜所见:杯状细胞细胞膜缺失,线粒体嵴模糊、髓样变;纤毛细胞、基底细胞、成纤维细胞细胞核膜不清,核固缩,染色质边集。丙二醇对照组气管组织和细胞结构与正常对照组相同。结论芥子气(2 mg/kg)可致大鼠气管组织和细胞急性损伤,组织损伤以黏膜上皮细胞脱落、灶性溃疡形成、黏膜下炎细胞浸润为特征,损伤程度随时间延长而加重。细胞损伤表现为杯状细胞细胞膜和细胞器损伤,纤毛细胞、基底细胞、成纤维细胞细胞核染色质损伤。
    • 刘洋; 孙艳彬; 许顺
    • 《中国医师杂志》  | 2017年
    • 摘要: 目的 总结颈段气管断裂的临床特点及诊疗经验,探讨合理的诊断策略及治疗方式.方法 回顾性分析中国医科大学附属第一医院2010年3月至2016年3月期间救治的21例颈段气管断裂患者的临床资料.观察患者诊疗过程及治疗结果.结果 21例颈段气管断裂患者,其中男18例(85.7%),女3例(14.3%);年龄16 ~58(中位年龄32)岁;其中开放性气管断裂10例(47.6%),闭合性气管断裂11例(52.4%).所有患者均经急诊抢救治疗,急诊治疗过程中患者因急性呼吸衰竭死亡2例,手术治疗过程因出现术中心跳骤停抢救无效死亡1例,其余手术过程均顺利,术后发生肺炎及肺不张并发症的患者6例(28.6%),术后随访6 ~48个月,现生存患者共16例(76.1%),术后4例闭合性气管断裂患者合并脊柱截瘫,其中2例因术后严重肺部炎症及经济负担放弃治疗,另2例工伤患者持续治疗中,但存在反复发作的肺炎,生活质量差.结论 颈段气管断裂是较为少见的严重胸外科急重症,处理方法相对简单,但与时间因素密切相关,充分的术前评估、尽早地急诊手术治疗及良好的术后治疗和护理对患者预后影响极大;同时开放性颈段气管断裂主要的危险因素是急诊抢救期间是否存在窒息及急性呼吸、循环系统衰竭情况发生,闭合性颈段气管断裂是否合并脊髓损伤是影响预后的重要因素.
    • 田艳艳; 黄细芝; 万玉娥; 李云秋
    • 《医学临床研究》  | 2015年
    • 摘要: [目的]观察先天性心脏病(简称先心病)合并重症肺炎患儿不同负压的吸痰效果,探讨不同年龄患儿吸痰的适宜负压.[方法]选择先心病合并肺炎患儿160例为研究对象,分为新生儿组、≤3岁组、>3岁组,吸痰前应用普米克令舒雾化吸入,按不同水平的负压吸痰,吸痰负压分别为≤80mmHg,80~150 mmHg,150~200mmHg,200~300 mmHg,记录患儿的心率(HR)、呼吸频率(RR)、血氧饱和度(SpO2)变化,同时观察气道黏膜损伤情况及吸痰时间.[结果]不同的吸痰负压对先心病合并肺炎患儿的HR、RR、SpO2、气道黏膜损伤均有影响,且年龄愈小,其最适负压愈低,新生儿吸痰负压宜低于80 mmHg,0~3岁负压控制在150 mmHg以下,3岁以上负压应控制在200 mmHg以内.[结论]先心病合并重症肺炎患儿吸痰,需根据不同年龄选择适宜的负压.
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