高温高湿环境下猫颅脑火器伤的病理学改变

目的 研究高温高湿环境下猫颅脑火器伤后病理学变化特点。方法 将杂种猫16只随机分为常温组、常温枪伤组、高温高湿组和高温高湿枪伤组，分别在光镜和电镜下观察其脑组织病理改变。结果 常温枪伤组早期表现为血管舒缩功能障碍，血管痉挛及扩张并存；高温高湿组血管痉挛减少，出血性表现增多；高温高湿枪伤组脑组织切片及超薄切片观察发现神经细胞存活数量明显减少，细胞器水肿变性，毛细血管紧密连接增宽，毛细血管破裂出血，髓鞘变性松解等病理变化，较常温颅脑火器伤中明显加重。结论 高温高湿环境对颅脑火器伤时的病理变化影响显著。     

高温高湿环境下猫颅脑火器伤后细菌生长特点

OBJECTIVE: To investigate the growth behavior of characteristics in craniocerebral gunshot wound of cats in a hot and humid environment. METHODS: Twenty-three cross-bred cats were randomly divided into 4 groups: group A, the gunshot wound control group at normal temperature, in which tissue sampling was performed immediately after the wounding; group B, another gunshot wound control group at normal temperature, in which the samples were taken 6 h after the wounding; group C, the gunshot wound group subjected to a hot and humid environment, in which the tissue samples were obtained 6 h after the wounding; group D, the control group without undergoing the wound. The tissues from the wound tract and the surrounding tissues were sampled for bacterial culture and counting. RESULTS: The bacterial counts of the tissues from the wound tract, the tissues within 5 mm and within 5-10 mm from wound tract varied insignificantly between groups A, B and C (P>0.05). In each group, the bacterial counts declined in the tissues as the distance of the sampling sites from the wound tract increased (P<0.01). The bacterial counts of the tissues from the wound tract and within 5 mm from the wound tract in group A, B and C were significantly different from those in group D (P<0.01). CONCLUSION: Hot and humid environment does not significantly affect the bacterial growth in the craniocerebral gunshot wound within the first 6 h, which is a safe period against rapid bacterial growth and suitable for debridement.     

高温高湿环境下犬贯通性颅脑火器伤模型的建立

目的 建立高温高湿环境下犬贯通性颅脑火器伤动物模型.方法 成年杂种犬40只,采用国产"54"式军用手枪,7.62mm手枪弹,枪口距犬额部10cm远处,冠状方向射击,制作颅脑贯通性火器伤模型.致伤后随机分为二组,即常温常湿组(对照组) 气温(Ta)(22.0±0.5)℃,相对湿度(RH)50%和高温高湿组(Ta) (39.0±0.5)℃,RH(80%～85%),每组20只.Powlab/8 sp生理记录仪动态监测体温、呼吸(R)、心率(HR)和平均动脉压(MAP)变化;监测血气分析和血电解质变化.结果 高温高湿环境下颅脑火器伤组伤情明显重于对照组,表现为生命体征紊乱,使呼吸明显加快,循环、体温调节功能衰竭;缩短了动物生存时间,增加动物的死亡率.结论 该动物模型对观察高温高湿环境下颅脑火器伤早期伤情变化特点是可行的、合理的,适应于高温高湿环境下颅脑火器伤的早期病理生理研究,并为该类创伤的早期救治提供实验依据.     

高温高湿环境下颅脑火器伤的基础与救治研究概论

较系统地介绍了高温高湿环境下颅脑火器伤的病理生理改变特点,指出高湿高湿环境是引起脑二次创伤的重要因素,是导致伤病员早期伤死的主要原因之一。提出加强这一军事医学课题研究、提高救治成功率的重要性。     

高温高湿环境下颅脑火器伤的基础与救治研究概论

较系统地介绍了高温高湿环境下颅脑火器伤的病理生理改变特点，指出高湿高湿环境是引起脑二次创伤的重要因素，是导致伤病员早期伤死的主要原因之一。提出加强这一军事医学课题研究、提高救治成功率的重要性。     

高温高湿环境肢体火器伤病理形态学变化

目的 通过建立高温高湿环境下犬肢体火器伤动物模型,探讨这一特殊环境下肢体火器伤的病理形态学变化,为其临床救治提供理论基础。方法 将８只杂种犬随机分为高温高湿组（５只）和常温常湿组（３只）,分别于火器伤后４、８、１２、２４h进行大体观察并通过光镜和电镜进行病理形态学观察。结果 大体观察可见高温高湿组６－８h后较常温常湿组道及肌肉变色区明显坟大,肢体肿胀加重,挫伤区色泽暗红,肌肉无收缩且有腐败臭味,有感染征;而常温常湿组１２－２４h伤道始出现臭味,光镜及电镜观察到高温高湿组各区肌肉纤维的病理变化均较常温常湿组显著,且损伤呈进行性加重,而常温常湿组的震荡区及震荡外区２４h伤道组织损伤均有减轻趋势。结论 高温高湿环境下肢体火器伤伤道肌肉组织病理损伤严重,且随时间的延长而逐渐加重,救治时尖强调早期彻底清创。     

亚低温治疗高温高湿环境下重型颅脑损伤的临床观察

目的观察亚低温治疗高温高湿环境下重型颅脑损伤的疗效,探讨亚低温治疗的平稳性和安全性。方法将200例高温高湿环境下重型颅脑损伤病人随机分为亚低温组(100例)和对照组(100例),亚低温组入院后或术后立即行亚低温治疗,酌情运用冬眠合剂、肌松剂和呼吸机,肛温控制在33℃~35℃,持续24h~5天。对照组行常规治疗。两组均观察颅内压(1CP)、生命体征、脑干听觉诱发电位(BAEP)I/V波幅比值等的变化。结果亚低温组经亚低温治疗后,ICP下降明显;23例血压下降,24例心率减慢,复温后以上指标均恢复正常;亚低温治疗后24h及复温后、双侧BAEPI/V比值与对照组同时间相比差异显著(P<0.05)。亚低温组死亡39例,死亡率39%;对照组死亡52例,死亡率52%,两组有显著性差异(P<0.05)。结论亚低温治疗高温高湿环境后重型颅脑伤能降低脑外伤后增高的ICP,从而使死亡率及致残率明显下降,亚低温治疗中合理使用辅助药物,可以保障亚低温治疗的平稳性和安全性。     

p38 MAPK在高温高湿环境下颅脑火器伤的变化

目的研究p38 MAPK在高湿环境下颅脑火器伤后活化及其原因。方法采用高温高湿颅脑枪伤模型,新西兰大白兔30只,随机分成常温[T(22.0±0.5)℃、RH50%]对照组,高温高湿[T(39.0±0.5)℃、RH80%~85%]枪伤后受热10、30 min,1、1.5、2 h组,每组5只。采用Western blot法检测脑匀浆p38 MAPK活性,应用化学发光和X线片显示,凝胶图像分析仪半定量分析。结果颅脑枪伤受高温高湿环境作用脑皮质和下丘脑的p38 MAPK的活性受湿热后迅速增高,于受热lh达高峰,随后下降。下丘脑的p38 MAPK活性比脑皮质高。结论高温高湿环境颅脑火器伤后p38X4APK活性早期明显升高,参与了脑的继发性损害过程。     

高温高湿环境兔颅脑火器伤后HSP70的变化

目的:研究热休克蛋白70(HSP70)在高温高湿环境下颅脑火器伤后的变化及其作用.方法:采用高温高湿颅脑枪伤模型,新西兰大白兔24只,随机分成常温对照组:(22.0±0.5)℃、RH 50%,常温枪伤组:(22.O±0.5)℃、RH 50%,高温高湿枪伤组(39.0±0.5)℃、RH 80%～85%,每组8只.采用Western blot法检测脑组织、淋巴细胞HSP70,应用化学发光和X线片显示,凝胶图像分析仪定量分析.结果:颅脑枪伤受高温高湿环境作用后,大脑皮层、下丘脑和淋巴细胞的HSP70显著增高;淋巴细胞中的HSP70与大脑皮层、下丘脑的变化趋势相一致.结论:脑组织和淋巴细胞中HSP70在高温高湿环境颅脑火器伤时显著增加.     

高温高湿环境颅脑火器伤后兔脑p38MAPK变化

OBJECTIVE: To study the activation of p38 mitogen-activated protein kinase (MAPK) in the brain of rabbits after craniocerebral gunshot injury in a hot and humid environment (HHE) and explore its possible mechanism. METHODS: Craniocerebral gunshot injury model was established in 30 New Zealand white rabbits, which were subsequently exposed to environment of normal temperature (at 22.0% +/- 0.5 degrees C; with relative humidity of 50%) or HHE at 39.0 +/- 0.5 degrees C; with relative humidity of 80%-85% for 10 min, 30 min, 1 h, 1.5 h, and 2 h groups, respectively, with 5 rabbits in each group. p38 MAPK activity in the brain tissues of the rabbits following the injury and environmental exposure were detected by Western blotting and analyzed semi-quantitatively by Bio-Profil gel image analysis system. RESULTS: p38 MAPK activity in the cortex and hypothalamus was significantly elevated following gunshot injury and HHE exposure, reaching the peak level at 1 h of HHE exposure and then decreased. p38 MAPK activity was significantly higher in the hypothalamus than in the cortex. CONCLUSION: p38 MAPK activity increases in the early stage following craniocerebral gunshot injury and HHE exposure in rabbits, the mechanism of which might involve the secondary brain insult.     

高温高湿环境肢体火器伤病理形态学变化

目的通过建立高温高湿环境下犬肢体火器伤动物模型,探讨这一特殊环境下肢体火器伤的病理形态学变化,为 其临床救治提供理论基础。方法将８只杂种犬随机分为高温高湿组（５只）和常温常温组（３只）,分别于火器伤后４、８、 １２、２４ ｈ进行大体观察并通过光镜和电镜进行病理形态学观察。结果大体观察可见高温高湿组６－８ ｈ后较常温常湿组 伤道及肌肉变色区明显扩大,肢体肿胀加重,挫伤区色泽暗红,肌肉无收缩且有腐败臭味,有感染征象;而常温常湿组 １２～２４ ｈ伤道始出现臭味。光镜及电镜观察到高温高湿组各区肌肉纤维的病理变化均较常温常湿组显著,且损伤呈进行 性加重,而常温常温组的震荡区及震荡外区２４ｈ伤道组织损伤均有减轻趋势。结论高温高湿环境下肢体火器伤伤道 肌肉组织病理损伤严重,且随时间的延长而逐渐加重,救治时更应强调早期彻底清创。     

高温高湿环境犬肢体火器伤后HSP70含量变化的实验研究

目的探讨高温高湿环境下肢体火器伤后热休克蛋白７０（ＨＳＰ７０）含量变化的规律。方法将１８只犬随机分为高温 高湿组、常温常湿组、热适应组,分别在致伤前及火器伤后ｌ、３、４、６、８、１０、１４、１８、２４ｈ检测外周血淋巴细胞和伤道骨骼 肌中ＨＳＰ７０含量。结果淋巴细胞中ＨＳＰ７０含量在高温高湿组的两个高峰分别为伤后４ｈ和ｌ４～ｌ８ｈ;热适应组３ｈ达 到高峰,持续至６ｈ;常温常湿组６ｈ达到高峰。常温常湿组伤道骨骼肌ＨＳＰ７０含量在伤后ｌ４～１８ｈ也出现一个增幅不 明显的高峰期。结论　高温高湿环境下肢体火器伤后ＨＳＰ７０含量的变化有其独特的规律。     

高温高湿环境犬肢体火器伤后超氧化物歧化酶和丙二醛含量的变化

目的探讨高温高湿环境下肢体火器伤后组织脂质过氧化与抗氧化酶变化的规律。方法将犬随机分为常温常湿组、热习服组、高温高湿组,分别在致伤前及火器伤后1、3、4、6、8、10、14、18、24h检测外周血和伤道骨骼肌中超氧化物歧化酶(SOD)和丙二醛(MDA)含量。结果(1)每组SOD、MDA的含量在伤后14h内呈正相趋势;(2)高温高湿组中MDA含量开始升高和其峰值的时间点提前,分别为3h和6h,峰值显著高于其他两组(P<0.05),SOD的含量则相反;(3)热习服组SOD含量较高温高湿组升高;(4)三组14h后SOD、18h后MDA含量无差异。结论高温高湿火器伤可使机体内脂质过氧化反应增强,热习服则明显减低这种作用。     

高温高湿环境下猫颅脑火器伤后细菌生长特点

目的研究高温高湿环境下猫颅脑火器伤后创面及周围组织细菌生长特点。方法杂种猫23只随机分为常温枪伤对照组(伤后立即取材,A组)、常温枪伤组(伤后6 h取材,B组)、高温高湿枪伤组(伤后6 h取材,C组)和空白对照组(D组),分别取创面及周围组织进行细菌培养并计数。结果A、B、C组其创面组织、伤道壁5 mm内组织、伤道壁5~10 mm内组织细菌含量无统计学差异(P>0.05),各组内随着离伤道距离的增加细菌含量减少(P<0.01)。3组创面组织、伤道壁5 mm内组织细菌含量与D组比较差异显著(P<0.01)。结论高温高湿环境对颅脑火器伤6 h内的细菌生长情况无显著影响,颅脑火器伤后6 h内细菌繁殖未进入高速增长期,进行清创仍是安全的。     

湿热环境猫颅脑火器伤早期脑微循环及血脑屏障的变化

目的 研究湿热环境对猫颅脑火器伤早期脑微循环的影响,为临床治疗提供实验依据。方法 24只成年猫用改良Carey法制作猫颅脑火器伤模型后,随机分为两组,每组12只,放入温度和相对湿度分别为25℃和50%,35℃和85%仿真模拟气候舱。通过脑微血管形态学及通透性和周围组织病理变化的观察,测定生命体征代偿指标、微血管中流动血液流变学特征和血脑屏障的变化来反应脑微循环的变化。结果 全部动物无死亡。两组动物在脑微血管形态学及通透性和周围组织病理变化显著;在生命体征指标、血液流变学特征和血脑屏障的损害程度上存在显著差异。结论 湿热环境对颅脑火器伤的早期脑微循环有显著影响,是颅脑火器伤的二次创伤。     

湿热环境下Ⅱ度烫伤大鼠施行冷却疗法后皮肤温度的改变

目的 观察大鼠浅Ⅱ度烫伤创面即刻施行冷疗后,在湿热环境下皮肤温度的变化。同时,评价冷疗敷料方法的降温效果。方法 24只Wistar大鼠,随机分成4组,即常温常湿对照组(常对组)、常温常湿冷疗组(常冷组)、湿热对照组(高对组)和湿热冷疗组(高冷组),每组6只。制作浅Ⅱ度烫伤模型后分别采取不同的干预条件,常温组的实验环境条件为干球温度(Tdb)(26.33±1.29)℃、相对湿度(rh)(71.05±4.57)%,湿热组的实验环境条件为Tdb(35.33±0.35)℃,rh(70.81±1.38)%,对照组不给予冷疗降温,冷疗组给予腹部冷疗敷料降温,暴露时间均为125min。监测皮肤温度(Ts),烫伤5min后每20min记录1次。结果 4组组内7个时间水平之间、不同时间水平组间以及不同组间比较,湿热环境使Ts升高(P<0.001),冷疗使Ts降低(P<0.001),且时间与环境温度(P≤0.002)、时间与冷疗(P<0.05)、时间、环境温度与冷疗对Ts变化影响有交互作用(P<0.05)。常温组冷疗前后Ts降低了(1.92±2.13)℃,湿热组Ts降低了(2.36±1.03)℃。结论 在湿热环境下,腹部冷疗敷料有效降低了大鼠创面皮肤温度,阻止了热损伤的进程和创面余热的不良作用。     

高温高湿环境下颅脑火器伤后兔脑HSP70变化

OBJECTIVE: To study the changes of heat shock protein 70 (HSP70) in the brain of rabbits with craniocerebral missile injury (CMI) and their impact on the injury in a hot and humid environment (HHE). METHODS: Twenty-four New Zealand white rabbits were randomized into 3 equal groups, namely normal temperature (NT) control group (subjected to treatment at temperature of 22.0+/-0.5 degrees C with relative humidity of 50%), NT gunshot group with CMI and HHE gunshot group with CMI. The rabbits in the latter two groups were subjected to normal temperature of 22.0+/-0.5 degrees C with relative humidity of 50% and environmental temperature of 39.0+/-0.5 degrees C with relative humidity of 80% to 85%, respectively, after establishment of CMI models. HSP70 in the brain tissues and lymphocytes was detected by Western blotting and visualized using chemoluminescence and X-ray films, followed by quantitative gel image analysis. RESULTS: Expressions of HSP70 in the cortex, hypothalamus and lymphocytes increased apparently in HHE gunshot group, and the changes of HSP70 in the lymphocytes were consistent with those in the cerebral cortex and hypothalamus. CONCLUSION: HSP70 expression in the brain tissues and the lymphocytes increase evidently after MCI in HHE.     

高温高湿环境下颅脑火器伤后兔脑HSP70变化

目的 研究高温高湿环境下颅脑火器伤后兔脑热休克蛋白70(HSP70)的变化及其作用。方法 采用高温高湿颅脑枪伤模型,24只新西兰大白兔随机分成常温(22.0±0.5℃、相对湿度50%)对照组、常温(22.0±0.5℃、相对温度50%)枪伤组和高温高湿(39.0±0.5℃、相对温度80%~85%)枪伤组,每组8只。采用Westernblot法检测脑组织、淋巴细胞中HSP70,应用化学发光和X线片显示,凝胶图像分析仪定量分析。结果 颅脑枪伤受高温高湿环境作用后,脑皮质、下丘脑和淋巴细胞的HSP70显著增高;淋巴细胞中的HSP70与大脑皮质、下丘脑的变化趋势相一致。结论 脑组织和淋巴细胞中HSP70在高温高湿环境颅脑火器伤时显著增加。