腹部创伤合并海水浸泡致重度体温过低症犬血液滤过复温的效果研究

目的 观察血液滤过不同复温速度对腹部创伤合并海水浸泡致重度体温过低症犬的救治效果,为海水浸泡伤员的救治提供理论基础和可行方案.方法 建立腹部创伤合并海水浸泡致重度体温过低症[(27.5±0.5)℃]致伤模型,按数字表法随机分为快速血滤复温组[8只,3℃/h复温至(38.0±0.5)℃]、慢速血滤复温组[8只,1.5 ℃/h复温至(38.0±0.5)℃]和体外复温组[5只,复温至(38.0±0.5)℃],复温过程中检测血生化、凝血功能和血气分析,同时观察各组死亡率.结果 血温35℃和38℃时,快速血滤复温组对外源性凝血途径凝血功能障碍(1.53±0.38,1.02±0.25)的纠正优于慢速血滤复温组(2.63±0.13,1.91±0.17) (P ＜0.05);血温32℃和35℃时,快速血滤复温组低钾血症[(2.90±0.51) mmol/L,(3.05 ±0.45) mmol/L]纠正逊于慢速血滤复温组[(3.42±0.94) mmol/L,(4.20±1.01) mmol/L](P ＜0.05).快速血滤复温组的死亡率为12.5％,慢速血滤复温组的死亡率为37.5％,体外复温组死亡率为100％.结论 对腹部创伤合并海水浸泡致重度体温过低症的患者,采用3℃/h的血液滤过复温可能更有利于提高救治效果和降低死亡率.     

不同复温方法对体温过低兔的复温作用研究

目的 观察3种不同复温方法对海水浸泡性体温过低兔的复温效果.方法 健康新西兰兔随机分为3组,每组10只,经(21.0±0.5)℃人工模拟海水浸泡免至肛温30℃,分别采用自然、水浴、复合碳纤维远红外线3种方法复温至肛温35℃,记录各组所用复温时间及复温以后体温下降度数.分别于浸泡前、复温前及复温3 h后静脉采血,测定血浆...     

兔肢体爆炸伤合并海水浸泡后在不同复温速率及维持浅低体温下机体炎症反应的特征

Objective To investigate effects of different rewarming rates and maintenance of light hypothermia on inflammatory response in rabbits after limb blast injury, coupled with seawater immersion. Methods First, the model of limb blast injury coupled with seawater immersion was reproduced [the animals were immersed to low body temperature of (31.0±0.5℃)]. Then, 24 adult rabbits were randomly divided into group Ⅰ [the rapid rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (8.94±0.93)℃/h], group Ⅱ [the slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (3.88±0.22)℃/h], group Ⅲ [another slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (2.18±0.12)℃/h], and the H group [the hypothermia group, n =6, rewarmed to (34 - 35)℃ at a rate of (4.49±0.66)℃/h and kept at that temperature till termination of the experiment]. Regulation of ambient temperature and warm transfusion were used to restore body temperature to target levels and maintained there for 6 hours. Blood samples were taken at 5 different times, I.e. Pre-injury time(T0), post-immersion time (T1), the time when rewarming started (T2), 3 h after rewarming (T3), and 6 h after rewarming (T4). Tissue samples from heart, liver, intestinum, lung and kidney were also collected. Levels of TNF-α (tumor necrosis factor-α), IL-1β (interleukin-1β) and IL-6 (interleukin-6) in plasma and MPO (myeloperoxidase) in homogenate were detected. Results Following rewarming, TNF-α, IL-1β, IL-6 concentrations in the plasma of the animals in group Ⅰ and group H were significantly higher when compared with those of the animals in group Ⅱ and group Ⅲ (P<0.05, P<0.01), and MPO activity in homogenate was significantly higher when compared with that of the animals in group Ⅱ and group Ⅲ(P<0.01, P<0.05), and no statistical difference could be seen between group Ⅱ and Ⅲ (P>0.05). Conclusions Rapid rewarming and maintenance of light hypothermia could obviously elevate TNF-α, IL-1β, IL-6 concentrations in plasma and MPO activity in homogenate, following limb blast injury coupled with hypothermia induced by seawater immersion, while slow rewarming (with a rewarming rate of 2-4℃/h) could significantly inhibit TNF-α, IL-1β, IL-6 levels and PMN activity.     

兔肢体爆炸伤合并海水浸泡后在不同复温速率及维持浅低体温下机体炎症反应的特征

Objective To investigate effects of different rewarming rates and maintenance of light hypothermia on inflammatory response in rabbits after limb blast injury, coupled with seawater immersion. Methods First, the model of limb blast injury coupled with seawater immersion was reproduced [the animals were immersed to low body temperature of (31.0±0.5℃)]. Then, 24 adult rabbits were randomly divided into group Ⅰ [the rapid rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (8.94±0.93)℃/h], group Ⅱ [the slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (3.88±0.22)℃/h], group Ⅲ [another slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (2.18±0.12)℃/h], and the H group [the hypothermia group, n =6, rewarmed to (34 - 35)℃ at a rate of (4.49±0.66)℃/h and kept at that temperature till termination of the experiment]. Regulation of ambient temperature and warm transfusion were used to restore body temperature to target levels and maintained there for 6 hours. Blood samples were taken at 5 different times, I.e. Pre-injury time(T0), post-immersion time (T1), the time when rewarming started (T2), 3 h after rewarming (T3), and 6 h after rewarming (T4). Tissue samples from heart, liver, intestinum, lung and kidney were also collected. Levels of TNF-α (tumor necrosis factor-α), IL-1β (interleukin-1β) and IL-6 (interleukin-6) in plasma and MPO (myeloperoxidase) in homogenate were detected. Results Following rewarming, TNF-α, IL-1β, IL-6 concentrations in the plasma of the animals in group Ⅰ and group H were significantly higher when compared with those of the animals in group Ⅱ and group Ⅲ (P<0.05, P<0.01), and MPO activity in homogenate was significantly higher when compared with that of the animals in group Ⅱ and group Ⅲ(P<0.01, P<0.05), and no statistical difference could be seen between group Ⅱ and Ⅲ (P>0.05). Conclusions Rapid rewarming and maintenance of light hypothermia could obviously elevate TNF-α, IL-1β, IL-6 concentrations in plasma and MPO activity in homogenate, following limb blast injury coupled with hypothermia induced by seawater immersion, while slow rewarming (with a rewarming rate of 2-4℃/h) could significantly inhibit TNF-α, IL-1β, IL-6 levels and PMN activity.     

兔肢体爆炸伤合并海水浸泡后在不同复温速率及维持浅低体温下机体炎症反应的特征

Objective To investigate effects of different rewarming rates and maintenance of light hypothermia on inflammatory response in rabbits after limb blast injury, coupled with seawater immersion. Methods First, the model of limb blast injury coupled with seawater immersion was reproduced [the animals were immersed to low body temperature of (31.0±0.5℃)]. Then, 24 adult rabbits were randomly divided into group Ⅰ [the rapid rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (8.94±0.93)℃/h], group Ⅱ [the slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (3.88±0.22)℃/h], group Ⅲ [another slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (2.18±0.12)℃/h], and the H group [the hypothermia group, n =6, rewarmed to (34 - 35)℃ at a rate of (4.49±0.66)℃/h and kept at that temperature till termination of the experiment]. Regulation of ambient temperature and warm transfusion were used to restore body temperature to target levels and maintained there for 6 hours. Blood samples were taken at 5 different times, I.e. Pre-injury time(T0), post-immersion time (T1), the time when rewarming started (T2), 3 h after rewarming (T3), and 6 h after rewarming (T4). Tissue samples from heart, liver, intestinum, lung and kidney were also collected. Levels of TNF-α (tumor necrosis factor-α), IL-1β (interleukin-1β) and IL-6 (interleukin-6) in plasma and MPO (myeloperoxidase) in homogenate were detected. Results Following rewarming, TNF-α, IL-1β, IL-6 concentrations in the plasma of the animals in group Ⅰ and group H were significantly higher when compared with those of the animals in group Ⅱ and group Ⅲ (P<0.05, P<0.01), and MPO activity in homogenate was significantly higher when compared with that of the animals in group Ⅱ and group Ⅲ(P<0.01, P<0.05), and no statistical difference could be seen between group Ⅱ and Ⅲ (P>0.05). Conclusions Rapid rewarming and maintenance of light hypothermia could obviously elevate TNF-α, IL-1β, IL-6 concentrations in plasma and MPO activity in homogenate, following limb blast injury coupled with hypothermia induced by seawater immersion, while slow rewarming (with a rewarming rate of 2-4℃/h) could significantly inhibit TNF-α, IL-1β, IL-6 levels and PMN activity.     

兔肢体爆炸伤合并海水浸泡后在不同复温速率及维持浅低体温下机体炎症反应的特征

Objective To investigate effects of different rewarming rates and maintenance of light hypothermia on inflammatory response in rabbits after limb blast injury, coupled with seawater immersion. Methods First, the model of limb blast injury coupled with seawater immersion was reproduced [the animals were immersed to low body temperature of (31.0±0.5℃)]. Then, 24 adult rabbits were randomly divided into group Ⅰ [the rapid rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (8.94±0.93)℃/h], group Ⅱ [the slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (3.88±0.22)℃/h], group Ⅲ [another slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (2.18±0.12)℃/h], and the H group [the hypothermia group, n =6, rewarmed to (34 - 35)℃ at a rate of (4.49±0.66)℃/h and kept at that temperature till termination of the experiment]. Regulation of ambient temperature and warm transfusion were used to restore body temperature to target levels and maintained there for 6 hours. Blood samples were taken at 5 different times, I.e. Pre-injury time(T0), post-immersion time (T1), the time when rewarming started (T2), 3 h after rewarming (T3), and 6 h after rewarming (T4). Tissue samples from heart, liver, intestinum, lung and kidney were also collected. Levels of TNF-α (tumor necrosis factor-α), IL-1β (interleukin-1β) and IL-6 (interleukin-6) in plasma and MPO (myeloperoxidase) in homogenate were detected. Results Following rewarming, TNF-α, IL-1β, IL-6 concentrations in the plasma of the animals in group Ⅰ and group H were significantly higher when compared with those of the animals in group Ⅱ and group Ⅲ (P<0.05, P<0.01), and MPO activity in homogenate was significantly higher when compared with that of the animals in group Ⅱ and group Ⅲ(P<0.01, P<0.05), and no statistical difference could be seen between group Ⅱ and Ⅲ (P>0.05). Conclusions Rapid rewarming and maintenance of light hypothermia could obviously elevate TNF-α, IL-1β, IL-6 concentrations in plasma and MPO activity in homogenate, following limb blast injury coupled with hypothermia induced by seawater immersion, while slow rewarming (with a rewarming rate of 2-4℃/h) could significantly inhibit TNF-α, IL-1β, IL-6 levels and PMN activity.     

兔肢体爆炸伤合并海水浸泡后在不同复温速率及维持浅低体温下机体炎症反应的特征

Objective To investigate effects of different rewarming rates and maintenance of light hypothermia on inflammatory response in rabbits after limb blast injury, coupled with seawater immersion. Methods First, the model of limb blast injury coupled with seawater immersion was reproduced [the animals were immersed to low body temperature of (31.0±0.5℃)]. Then, 24 adult rabbits were randomly divided into group Ⅰ [the rapid rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (8.94±0.93)℃/h], group Ⅱ [the slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (3.88±0.22)℃/h], group Ⅲ [another slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (2.18±0.12)℃/h], and the H group [the hypothermia group, n =6, rewarmed to (34 - 35)℃ at a rate of (4.49±0.66)℃/h and kept at that temperature till termination of the experiment]. Regulation of ambient temperature and warm transfusion were used to restore body temperature to target levels and maintained there for 6 hours. Blood samples were taken at 5 different times, I.e. Pre-injury time(T0), post-immersion time (T1), the time when rewarming started (T2), 3 h after rewarming (T3), and 6 h after rewarming (T4). Tissue samples from heart, liver, intestinum, lung and kidney were also collected. Levels of TNF-α (tumor necrosis factor-α), IL-1β (interleukin-1β) and IL-6 (interleukin-6) in plasma and MPO (myeloperoxidase) in homogenate were detected. Results Following rewarming, TNF-α, IL-1β, IL-6 concentrations in the plasma of the animals in group Ⅰ and group H were significantly higher when compared with those of the animals in group Ⅱ and group Ⅲ (P<0.05, P<0.01), and MPO activity in homogenate was significantly higher when compared with that of the animals in group Ⅱ and group Ⅲ(P<0.01, P<0.05), and no statistical difference could be seen between group Ⅱ and Ⅲ (P>0.05). Conclusions Rapid rewarming and maintenance of light hypothermia could obviously elevate TNF-α, IL-1β, IL-6 concentrations in plasma and MPO activity in homogenate, following limb blast injury coupled with hypothermia induced by seawater immersion, while slow rewarming (with a rewarming rate of 2-4℃/h) could significantly inhibit TNF-α, IL-1β, IL-6 levels and PMN activity.     

兔肢体爆炸伤合并海水浸泡后在不同复温速率及维持浅低体温下机体炎症反应的特征

Objective To investigate effects of different rewarming rates and maintenance of light hypothermia on inflammatory response in rabbits after limb blast injury, coupled with seawater immersion. Methods First, the model of limb blast injury coupled with seawater immersion was reproduced [the animals were immersed to low body temperature of (31.0±0.5℃)]. Then, 24 adult rabbits were randomly divided into group Ⅰ [the rapid rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (8.94±0.93)℃/h], group Ⅱ [the slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (3.88±0.22)℃/h], group Ⅲ [another slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (2.18±0.12)℃/h], and the H group [the hypothermia group, n =6, rewarmed to (34 - 35)℃ at a rate of (4.49±0.66)℃/h and kept at that temperature till termination of the experiment]. Regulation of ambient temperature and warm transfusion were used to restore body temperature to target levels and maintained there for 6 hours. Blood samples were taken at 5 different times, I.e. Pre-injury time(T0), post-immersion time (T1), the time when rewarming started (T2), 3 h after rewarming (T3), and 6 h after rewarming (T4). Tissue samples from heart, liver, intestinum, lung and kidney were also collected. Levels of TNF-α (tumor necrosis factor-α), IL-1β (interleukin-1β) and IL-6 (interleukin-6) in plasma and MPO (myeloperoxidase) in homogenate were detected. Results Following rewarming, TNF-α, IL-1β, IL-6 concentrations in the plasma of the animals in group Ⅰ and group H were significantly higher when compared with those of the animals in group Ⅱ and group Ⅲ (P<0.05, P<0.01), and MPO activity in homogenate was significantly higher when compared with that of the animals in group Ⅱ and group Ⅲ(P<0.01, P<0.05), and no statistical difference could be seen between group Ⅱ and Ⅲ (P>0.05). Conclusions Rapid rewarming and maintenance of light hypothermia could obviously elevate TNF-α, IL-1β, IL-6 concentrations in plasma and MPO activity in homogenate, following limb blast injury coupled with hypothermia induced by seawater immersion, while slow rewarming (with a rewarming rate of 2-4℃/h) could significantly inhibit TNF-α, IL-1β, IL-6 levels and PMN activity.     

兔肢体爆炸伤合并海水浸泡后在不同复温速率及维持浅低体温下机体炎症反应的特征

Objective To investigate effects of different rewarming rates and maintenance of light hypothermia on inflammatory response in rabbits after limb blast injury, coupled with seawater immersion. Methods First, the model of limb blast injury coupled with seawater immersion was reproduced [the animals were immersed to low body temperature of (31.0±0.5℃)]. Then, 24 adult rabbits were randomly divided into group Ⅰ [the rapid rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (8.94±0.93)℃/h], group Ⅱ [the slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (3.88±0.22)℃/h], group Ⅲ [another slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (2.18±0.12)℃/h], and the H group [the hypothermia group, n =6, rewarmed to (34 - 35)℃ at a rate of (4.49±0.66)℃/h and kept at that temperature till termination of the experiment]. Regulation of ambient temperature and warm transfusion were used to restore body temperature to target levels and maintained there for 6 hours. Blood samples were taken at 5 different times, I.e. Pre-injury time(T0), post-immersion time (T1), the time when rewarming started (T2), 3 h after rewarming (T3), and 6 h after rewarming (T4). Tissue samples from heart, liver, intestinum, lung and kidney were also collected. Levels of TNF-α (tumor necrosis factor-α), IL-1β (interleukin-1β) and IL-6 (interleukin-6) in plasma and MPO (myeloperoxidase) in homogenate were detected. Results Following rewarming, TNF-α, IL-1β, IL-6 concentrations in the plasma of the animals in group Ⅰ and group H were significantly higher when compared with those of the animals in group Ⅱ and group Ⅲ (P<0.05, P<0.01), and MPO activity in homogenate was significantly higher when compared with that of the animals in group Ⅱ and group Ⅲ(P<0.01, P<0.05), and no statistical difference could be seen between group Ⅱ and Ⅲ (P>0.05). Conclusions Rapid rewarming and maintenance of light hypothermia could obviously elevate TNF-α, IL-1β, IL-6 concentrations in plasma and MPO activity in homogenate, following limb blast injury coupled with hypothermia induced by seawater immersion, while slow rewarming (with a rewarming rate of 2-4℃/h) could significantly inhibit TNF-α, IL-1β, IL-6 levels and PMN activity.     

兔肢体爆炸伤合并海水浸泡后在不同复温速率及维持浅低体温下机体炎症反应的特征

Objective To investigate effects of different rewarming rates and maintenance of light hypothermia on inflammatory response in rabbits after limb blast injury, coupled with seawater immersion. Methods First, the model of limb blast injury coupled with seawater immersion was reproduced [the animals were immersed to low body temperature of (31.0±0.5℃)]. Then, 24 adult rabbits were randomly divided into group Ⅰ [the rapid rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (8.94±0.93)℃/h], group Ⅱ [the slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (3.88±0.22)℃/h], group Ⅲ [another slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (2.18±0.12)℃/h], and the H group [the hypothermia group, n =6, rewarmed to (34 - 35)℃ at a rate of (4.49±0.66)℃/h and kept at that temperature till termination of the experiment]. Regulation of ambient temperature and warm transfusion were used to restore body temperature to target levels and maintained there for 6 hours. Blood samples were taken at 5 different times, I.e. Pre-injury time(T0), post-immersion time (T1), the time when rewarming started (T2), 3 h after rewarming (T3), and 6 h after rewarming (T4). Tissue samples from heart, liver, intestinum, lung and kidney were also collected. Levels of TNF-α (tumor necrosis factor-α), IL-1β (interleukin-1β) and IL-6 (interleukin-6) in plasma and MPO (myeloperoxidase) in homogenate were detected. Results Following rewarming, TNF-α, IL-1β, IL-6 concentrations in the plasma of the animals in group Ⅰ and group H were significantly higher when compared with those of the animals in group Ⅱ and group Ⅲ (P<0.05, P<0.01), and MPO activity in homogenate was significantly higher when compared with that of the animals in group Ⅱ and group Ⅲ(P<0.01, P<0.05), and no statistical difference could be seen between group Ⅱ and Ⅲ (P>0.05). Conclusions Rapid rewarming and maintenance of light hypothermia could obviously elevate TNF-α, IL-1β, IL-6 concentrations in plasma and MPO activity in homogenate, following limb blast injury coupled with hypothermia induced by seawater immersion, while slow rewarming (with a rewarming rate of 2-4℃/h) could significantly inhibit TNF-α, IL-1β, IL-6 levels and PMN activity.     

远红外线救治海水浸泡性体温中度过低症兔复温效果试验

目的:利用远红外线对海水浸泡性体温中度过低症兔进行复温,观察其复温速度、体温后降幅度及血浆IL-8变化,与现有复温方法比较,综合评价其复温效果。方法:将30只健康新西兰兔随机分为3组:自然组、水浴组和远红外线组,每组10只。将家兔浸泡于(21.0±0.5)℃人工海水中至肛温30℃,制备海水浸泡性体温中度过低症动物模型。分别采用自然、水浴、远红外线3种方法对其进行复温,记录体温后降幅度,以及兔肛温恢复至35℃时各组所用复温时间。复温3 h自颈内静脉采血,测定血浆IL-8含量。结果:各组间复温时间、体温后降幅度、复温3 h血浆IL-8含量均有统计学差异(P<0.01)。结论:远红外线复温法是一种有效救治海水浸泡性体温过低症的方法,具有复温速度适中、体温后降幅度小、血浆IL-8表达少等优点,安全有效复温的同时兼具机体保护作用。     

超声心动图在低温后复温兔左心功能评价中价值

目的探讨超声心动图评价兔低温后复温心功能的价值。方法将20只兔随机分为4组,每组各5只。第1组在室温条件下不做任何处理,为常温组;第2组置于低温环境(-23~-17℃)8 h,为低温组;第3、4组置于低温环境下8 h,并分别置于室温环境下复温2 h和4 h,分别设为复温2 h组与复温4 h组。应用超声心动图仪测量各组射血分数(EF)、舒张末期容积(EDV)、收缩末期容积(ESV)、短轴缩短率(FS)及等容舒张时间(IVRT);应用组织多普勒超声诊断技术(TDI)检测各组兔心脏在心尖四腔心切面上室间隔侧的二尖瓣环舒张早期的峰值运动速度(Em)以及收缩期的峰值运动速度(Sm)。超声测量后,从耳缘静脉取血测量肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)及超敏C反应蛋白测定(h CRP)。检查、测量结束后,各组兔均处死,并每组随机取1只兔,取其左室心尖部心肌观察病理改变。结果超声心动图显示,20只兔中有1只兔为房间隔缺损,故最后纳入统计分析的动物数量为19只。对4组兔的EF、EDV、ESV、FS值分别进行两两比较发现,差异均无统计学意义(P>0.05);低温组、复温2 h组、复温4 h组的IVRT均高于常温组,差异均有统计学意义(P<0.05);复温2 h组、复温4 h组、低温组的IVRT值进行两两比较,差异均无统计学意义(P>0.05)。低温组、复温2 h组、复温4 h组的Em、Sm值均低于常温组,差异均有统计学意义(P<0.05);低温组、复温2 h组、复温4 h组的Em、Sm值两两比较,差异均无统计学意义(P>0.05)。低温组、复温2 h组、复温4 h组的CK、LDH均明显高于常温组,但4组兔的CK、CK-MB、LDH及h CRP组间两两比较,差异均无统计学意义(P>0.05)。结论超声心动图可较早的反应低温后复温对于兔左心功能的影响,可有助于临床早期诊断。     

大鼠腹部开放伤合并海水浸泡后内毒素、TNF-α、IL-6、IL-8的变化

目的：观察大鼠腹部开放伤合并海水浸泡后不同时段血浆内毒素（LPS）、肿瘤坏死因子-α（TNF-α）、IL-6和IL-8的变化。方法：成年健康Wistar大鼠116只,随机分为2组,其中腹部开放伤合并海水浸泡组96只,腹部开放伤对照组20只。应用微生物快速检测仪和γ测量仪检测大鼠腹部开放伤合并海水浸泡后0.5,1,2,3和4h血浆LPS、TNF-α、IL-6和IL-8水平。结果：腹部开放伤合并海水浸泡2～4h后,血浆中LPS水平明显上升,与对照组比较具有显著性差异。海水浸泡4h后血浆中TNF-α浓度上升明显,具有显著性差异。海水浸泡3～4h后血浆中IL-6浓度明显升高,具有显著性差异。海水浸泡后不同时间血浆中IL-8浓度与对照组比较无明显变化。结论：血浆中LPS、TNF-α和IL-6浓度明显升高与损伤关系密切,是引发中毒性休克导致机体死亡的主要原因之一。     

治疗性低温及其诱导时机对兔复苏后心肌的影响

目的观察不同时机行轻度低温干预对室颤兔心肌组织能量、超微结构和血清心肌肌钙蛋白(cTNI)、肿瘤坏死因子α(TNF-α)水平以及近期死亡率的影响。方法雄性新西兰兔54只,随机分为5组:常温(39.0±0.5℃)对照组(n=8),低温(33.5±0.5℃)对照组(n=8),常温(39.0±0.5℃)复苏组(n=14),复苏前低温(33.5±0.5℃)组(n=10),复苏后低温(33.5±0.5℃)组(n=14)。采用心外膜电刺激致颤法制备兔心肺复苏模型。复苏后4h采血检测血清cTNI、TNF-α水平;低温各组均持续控温4h后自然复温,观察各组存活情况至复苏后48h,将兔处死后行左室心尖组织电镜检查和三磷腺苷(ATP)、二磷酸腺苷(ADP)、磷酸腺苷(AMP)含量测定,计算心肌能荷(EC)。结果复苏后低温组和两对照组48h存活率均为100%,高于常温复苏组和复苏前低温组(60.0%和44.4%,P<0.05),复苏前低温组48h存活率低于常温复苏组(P<0.05)。各复苏组血清cTNI水平均高于两对照组,复苏前低温组血清cTNI水平低于常温复苏组和复苏后低温组(P<0.05);常温复苏组血清TNF-α水平明显高于其他各组(P<0.05),两低温复苏组间及两对照组间无统计学差异(P>0.05)。复苏前和复苏后低温组心肌组织ATP含量均高于常温复苏组,复苏后低温组和常温复苏组心肌组织ATP含量均较对照组明显减低(P<0.05);常温复苏组EC明显低于两对照组和复苏前低温组(P<0.05);复苏后低温组EC与复苏前低温组及两对照组间无统计学差异(P>0.05)。复苏前和复苏后低温组复苏后48h心肌超微结构损害均较常温复苏组轻(P<0.05)。结论室颤兔自主循环恢复后存在心肌组织损害和能量代谢异常;自主循环恢复后轻度低温干预可减轻心肌组织结构损害,降低48h死亡率,其保护机制与改善心肌细胞能量代谢、抑制炎症反应有关;室颤前轻度低温处理不能降低48h死亡率。     

血清TNF-α、IL-6检测对慢性充血性心衰的临床价值

目的探讨慢性充血性心力衰竭(chronic congestive heart failure,CHF)患者血清中肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)检测的价值。方法用放射免疫方法测定176例CHF患者和30例健康人血清中TNF-α、IL-6水平。比较分析CHF患者与正常人以及不同心功能程度的CHF患者之间TNF-α、IL-6水平的变化。结果CHF患者血清中TNF-α、IL-6水平明显高于正常对照组(P<0.05),且均随着心衰程度的加重而增高,呈高度正相关。不同程度心衰患者之间TNF-α、IL-6水平均有明显差异(P<0.01)。结论CHF患者存在免疫激活和心肌炎症反应,心衰程度越重,炎症反应也越明显。放射免疫方法测定TNF-α、IL-6对CHF病程及治疗疗效预后判断具有重要的价值。     

帕瑞昔布钠超前镇痛对颌面外科手术患者炎性细胞因子和凝血功能的影响

目的观察帕瑞昔布钠超前镇痛对颌面外科手术患者炎性细胞因子和凝血功能的影响。方法将60例在全麻下行颌面外科手术患者随机分为Ⅰ、Ⅱ两组,每组30例:Ⅰ组于手术开始前30 min静脉注射帕瑞昔布钠40 mg,Ⅱ组静脉注射生理盐水10 ml,术中给予靶控输注丙泊酚和瑞芬太尼静脉全麻,维持其血浆浓度分别为3.5～5.0 mg/L和3.0μg/L。于麻醉诱导前(T1)、术毕(T2)、术后6 h(T3)、术后24 h(T4)测定血浆TNF-α、IL-6、IL-10浓度及出凝血时间,记录术毕即刻、术后6、24 h视觉模拟镇痛评分(visual analogue scale,VAS)。结果术毕及术后6h VAS评分Ⅰ组为(1.8±0.7)分和(2.1±0.8)分,显著低于Ⅱ组(2.9±0.9)分和(3.8±0.8)分(P<0.05);术后24 h VAS评分两组差异无统计学意义(P>0.05);两组T2～4时TNF-α、IL-6、IL-10水平均较T1时明显升高(P<0.05);Ⅰ组与Ⅱ组比较,T2～4时TNF-α、IL-6水平明显降低(P<0.05),IL-10水平明显升高(P<0.05);两组凝血功能比较差异无统计学意义(P>0.05)。结论帕瑞昔布钠超前镇痛效果好,能减轻手术引起的过度炎性反应且不影响凝血功能。     

血浆TGF-β、TNF-α及IL-10水平在预测放射性肺炎中的价值研究

目的 探讨接受放疗的胸部肿瘤患者血液中TNF-α、TGF-β、IL-10水平变化与放射性肺炎(RP)的关系。方法 对69例接受三维适形放疗的Ⅲ期肺癌或食管癌患者采用酶联免疫吸附实验法于放疗前、放疗剂量达40~50 Gy时及放疗后检测血浆中TNF-α、TGF-β和IL-10水平,并计算IL-10/TNF-α比值。结果 28例患者发生RP。RP者中放疗前TGF-β、TNF-α、IL-10和IL-10/TNF-α分别为(15.2±13.4)μg/L、(28.4±13.4)、(24.1±17.1)ng/L和1.01±0.86;放疗中TNF-α升高达(36.1±15.5)ng/L(t=2.01,P=0.040),IL-10下降达(18.8±10.8)ng/L(t=1.40,P=0.166),IL-10/TNF-α下降为0.62±0.55(t=1.90,P=0.063);放疗后TNF-α高于放疗前[(36.9±15.5)ng/L;t=-2.20,P=0.032],IL-10和IL-10/TNF-α分别为(13.7±6.2)ng/L和0.41±0.21,明显低于放疗前(t=3.03,P=0.005;t=3.60,P=0.001);TGF-β在放疗前、中、后均相似(P＞0.05)。在无RP者中放疗前TGF-β、TNF-α、IL-10和IL-10/TNF-α与放疗中、后均相似(P＞0.05)。RP者与无RP 者中放疗前TGF-β相似(t=0.54,P=0.594),放疗中前者TNF-α明显高于后者(t=2.02,P=0.048),放疗后前者IL-10和IL-10/TNF-α明显低于后者(t=2.50,P=0.015;t=4.63,P=0.000)。结论 TNF-α和IL-10水平变化与RP发生密切相关,动态监测其变化可早期预测RP发生,可作为急性放射性肺损伤易感性指标。     

腹部开放伤合并人工海水浸泡大鼠肠道免疫屏障功能的变化

目的 探讨腹部开放伤合并人工海水浸泡大鼠肠道免疫屏障功能的变化及意义.方法 建立腹部开放伤合并人工海水浸泡大鼠致伤模型.50只Wistar大鼠随机分为5组,每组10只.A组:腹部开放伤合并海水浸泡组;B组:单纯腹部开放伤组;C组:单纯海水浸泡组;D组:腹部开放伤合并生理盐水浸泡组;E组:正常对照组.观察腹腔海水浸泡后肠内容物sIsA及血浆IgA、内毒素(LPS)、肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)含量变化及血、肝脏、肠系膜淋巴结细菌定量培养情况;观察HE染色小肠组织病理损伤评分.结果 与E组比较,A组肠内容物SIgA、血浆IgA含量显著下降;血浆LPS、TNF-α、IL-6含量显著升高;发生肠道细菌易位(P＜0.05或P＜0.01);HE染色显示小肠黏膜组织出现不同程度的损伤(P＜0.05或P＜0.01).结论 腹部开放伤合并海水浸泡后肠道免疫屏障功能显著下降,与内毒素血症和肠道细菌易位的发生密切相关,炎症因子释放及肠黏膜屏障功能损伤是肠道免疫屏障功能受损的重要机制之一.     

丹参酮ⅡA对小鼠肺爆震伤导致的脑损伤的保护作用

 目的 探讨丹参酮ⅡA(Tan ⅡA)对小鼠肺爆震伤导致的脑损伤的保护作用。方法 建立小鼠肺爆震伤致脑损伤模型。将30只C57BL/6小鼠随机分为对照组(Sham)、肺爆震伤组(Blast)和Tan ⅡA干预组,每组10只。冲击伤后48 h采集标本,通过HE和ROS染色观察脑组织病理改变,Western blot检测脑损伤标志物Tau和S100β,炎性相关因子IL-1β、TNF-α和IL-10,氧化应激相关因子SOD-1、IRE-α和MDA5,以及PI3K、p-PI3K、Akt、p-Akt和NF-κB的表达情况。结果 蛋白结果显示,与Sham组相比,Blast组S100β升高到(31.5±4.19),其他相关促进因子均升高,而通路上NF-κB升高到(12.25±1.92),PI3K和Akt的磷酸化分别升高到(4.36±0.41)和(27.00±0.09),而与Blast组相比,Tan ⅡA组S100β降低到(0.21±0.09),Tan ⅡA恢复了冲击波导致的相关因子改变,NF-κB降低到(0.32±0.02),PI3K和Akt的磷酸化分别降低到(0.47±0.01)和(0.18±0.04),上述差异均具有统计学意义(P＜0.05)。结论 Tan ⅡA对肺爆震伤导致的脑损伤具有保护作用,其机制可能是通过抑制PI3K/Akt/NF-κB信号通路来实现的。     

脑梗死患者血同型半胱氨酸与炎症因子及神经功能缺损相关性研究

目的探讨脑梗死(CI)患者血同型半胱氨酸(Hcy)与炎症因子及神经功能缺损的相关性。方法收集2015年2月至2016年3月就诊的首次发病的CI患者90例,为CI组;选取同期于健康体检中心体检的健康人群90例,为对照组(C组)。检测血清中Hcy、高敏C反应蛋自(hs-CRP)、肿瘤坏死因子(TNF-α)、白细胞介素(IL)-1β、IL-6及IL-10;记录患者临床神经功能缺损评分(CNDS)评分;分析Hcy与炎症因子、CNDS的相关性。结果与C组比较,CI组患者血清中Hcy[(23.57±8.64)μmol/L比(9.89±4.58)μmol/L]、hs-CRP[(4.32±1.41)mg/L比(0.69±0.31)mg/L]、TNF-α[(31.24±6.34)pg/ml比(6.15±2.59)pg/ml]、IL-1β[(1.31±0.25)pg/ml比(0.34±0.11)pg/ml]、IL-6[(15.62±3.59)pg/ml比(2.19±1.42)pg/ml]均显著升高,IL-10[(5.19±2.13)pg/ml比(15.12±3.42)pg/ml]显著降低,差异均有统计学意义(P<0.01)。根据CNDS评分标准,将CI组患者分为3个亚组,其中,CI轻度组23例,CI中度组36例,CI重度组31例;与C组比较,CI组3个亚组患者CNDS评分均显著升高(P<0.05)。相关性分析显示,Hcy与hs-CRP、TNF-α、IL-1β、IL-6呈正相关(Rs>0,P<0.05),与IL-10呈负相关(Rs<0,P<0.05)。血清中Hcy与CI轻度、中度患者的CNDS评分呈正相关(r=0.691、r=0.632,P<0.05),而重度患者CNDS评分与血清中Hcy无相关性(r=0.049,P>0.05)。结论 CI患者血清中Hcy与炎症因子及神经功能缺损具有相关性,可反应CI患者的炎症状态和病情的严重程度。