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1.
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.  相似文献   

2.
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.  相似文献   

3.
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.  相似文献   

4.
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.  相似文献   

5.
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.  相似文献   

6.
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.  相似文献   

7.
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.  相似文献   

8.
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.  相似文献   

9.
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.  相似文献   

10.
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.  相似文献   

11.
目的复制冲击波和液体火箭推进剂中毒致冲毒复合伤的动物模型。方法健康雄性Wistar大鼠392只,随机分为7组①冲击伤组;②偏二甲基肼(UDMH)组;③四氧化二氮(N  相似文献   

12.
目的:探讨模拟实战条件下的动物爆炸冲击性损伤及脊髓爆炸冲击后的病理变化。方法:采用60 kg TNT当量的温压弹在1∶1军舰船舱模型内引爆后,现场尸检分析动物的致死原因,利用组织病理切片技术和透射电子显微镜技术观察脊髓的爆炸冲击损伤的病理特征。结果:爆炸后实验动物大部分死亡,暂时存活的动物也在1 h内死亡;动物的冲击损伤的死亡原因主要是体内重要脏器的挫裂伤;单纯脊髓冲击损伤,可以损伤脊髓内血管而造成脊髓出血、缺血性损伤;病理切片和电镜照片显示:脊髓损伤主要是白质结构的异常,水肿及脱髓鞘改变,以及神经元细胞核浓聚、偏位甚至破裂。结论:爆炸冲击性损伤多由于脏器伤情严重而掩盖了脊髓损伤的表现,脊髓爆炸冲击损伤是战伤中不可忽视的部分。  相似文献   

13.
目的摸索爆炸冲击波导致脊髓损伤的超压范围,建立实验室条件下脊髓爆震伤模型,探讨脊髓爆震伤的致伤特点。方法采用10 g的单质锰炸药(RDX)为水下爆源,随机取18只大鼠,通过手术将脊髓暴露后,将大鼠固定于封水仓内,仅椎板切除段脊髓外露于冲击波作用之下,最后按照冲击波到达脊髓表面的超压峰值为10、5、3 MPa分为3组致伤,同时检测冲击波的正压作用时间。另将12只大鼠随机分为致伤组和对照组,致伤组大鼠按照已选定的冲击波超压强度下爆炸致伤,观察伤后全身及脊髓的病理学变化。结果水下爆炸距离0.3、0.8、1.5 m测得的冲击波超压峰值分别为10、5、3 MPa,冲击波超压峰值为3 MPa时可造成大鼠双后肢运动诱发电位(motor evoked potential,MEP)潜伏期延长1.0 ms或波幅下降50%,而不致大鼠死亡。病理学显示脊髓内可见大量散在的出血坏死灶。结论水下爆炸冲击波超压峰值为3 MPa时,能够建立大鼠开放式可控性脊髓爆震伤模型。  相似文献   

14.
目的 分析经后路减压复位固定治疗中上胸椎骨折的可行性及手术特点。 方法 对17例中上胸椎骨折患者进行回顾性研究,统计并发症的发生,比较手术前后脊髓完全性损伤和不完全性损伤的功能状态,观察脊髓无损伤患者有无医源性损伤。 结果 术后无手术并发症发生。不完全性损伤6例(不完全性损伤组),随访时美国脊髓损伤协会(ASIA)脊髓功能分级提高1~3级;完全性损伤8例(完全性损伤组),随访时ASIA分级无提高。完全性与不完全性损伤组手术前后感觉评分间差异有统计学意义(F =476.47,P=0.000)。手术前后运动评分之间差异有统计学意义(F=46.75,P =0.000)。脊髓功能正常3例,随访时ASIA分级无降低,感觉和运动评分无变化。 结论 对于中上胸椎骨折患者,后人路手术能避免加重胸部合并伤及其他组织系统的合并伤,可以在骨折早期安全、有效解除包括椎管前方的脊髓压迫,从而有利于脊髓功能的恢复。  相似文献   

15.
The spinal cord is one of the most commonly affected sites in decompression sickness (DCS). Alternative methods have long been sought to protect against DCS spinal cord dysfunction, especially when hyperbaric treatment is unavailable. Use of perfluorocarbon (PFC) emulsion with or without oxygen breathing has shown survival benefits in DCS animal models. The effectiveness of intravenous PFC emulsion with oxygen breathing on spinal cord function was studied. Somatosensory-evoked potentials (SSEPs) and histologic examination were chosen to serve as measures. After fast decompression (203 kPa/minute) from 709 kPa (for 60 minutes), male Sprague-Dawley rats randomly received: 1) air and saline; 2) oxygen (O2) and saline; 3) O2 and PFC emulsion. The incidence and average number of abnormal SSEP waves in survival animals that received O2 and PFC emulsion were significantly reduced (P < 0.05). Foci of demyelination, necrosis and round non-staining defects in white matter regions of the spinal cord could be found in severe DCS rats. We concluded that administration of PFC emulsion combined with oxygen breathing was beneficial for DCS spinal conductive dysfunction in rats.  相似文献   

16.
水下冲击波与空气冲击波对生物内脏损伤效应的对比研究   总被引:4,自引:0,他引:4  
目的对比研究水下冲击波与空气冲击波对生物内脏的损伤效应,为其防治提供一定的依据。方法用1000g TNT分别进行水下和空气中爆炸,压力传感器测定冲击波的物理参数,包括峰值压力、正向持续时间和冲量。取成年杂种犬26只,其中水下爆炸20只,空气中爆炸6只,分别用1000g TNT进行水下和空气中爆炸,观察伤后6h动物存活情况和病理形态学改变。结果水下冲击波的峰值压力明显高于空气冲击波的峰值压力,尽管正向持续时间比空气冲击波短,但冲量仍明显大于空气冲击波。生物效应的测定结果表明,水下冲击波引起的死亡率高(50%),致死边界远(距爆心12.5m),肺和腹腔脏器损伤的发生率高,且伤情严重,而空气冲击波引起的损伤轻微,仅个别动物有轻微肺损伤,未见动物死亡。结论同质量TNT水下和空气中爆炸,水下冲击波的峰值压力和冲量明显高于空气冲击波,对生物的杀伤效应也明显强于空气冲击波,肺和腹腔脏器的损伤是早期救治的重要环节。  相似文献   

17.
目的 观察不同压力的高压氧(HBO)对大鼠脊髓损伤(spinal cord injury,SCI)后细胞凋亡的影响,探讨HBO治疗SCI的最佳压力.方法 90只SD大鼠采用Allen's打击法造成SCI后随机分为5组:对照组(A组)、0.15 MPa HBO组(B组)、0.20 MPa HBO组(C组)、0.22 MPa HBO组(D组)和0.25 MPa HBO组(E组).损伤后第3、7、14天分别对5组大鼠进行取材,采用Tunel法检测凋亡细胞,光镜下观察,并对结果进行统计学分析;神经功能评价采用开放场地实验评估大鼠后腿运动功能(BBB评分).结果 与A组比较,HBO各压力组在3个时间点凋亡的细胞数有所减少,神经功能有所改善,且差异有统计学意义(P<0.05).与B组比较,C、D和E组凋亡的细胞数有所减少,BBB评分改善,且差异有统计学意义(P<0.05).与C组比较,E组于第3和第7天的差异有统计学意义(P<0.05);第14天的差异无统计学意义(P>O.05).结论 HBO能抑制SCI后细胞的凋亡,其作用在一定范围内与压力的升高相关.
Abstract:
Objective To study the effects of HBO at different pressures on apoptosis following spinal cord injury in rats and also to investigate ideal pressure value of hyperbaric oxygen(HBO) on spinal cord injury (SCI). Methods The SCI model was established with Allen's weight dropping by using 90 SD rats. Then, the animals were randomly divided into 5 groups following SCI: the control group ( group A); the HBO treatment group at 0. 15 Mpa (group B); the HBO treatment group at 0. 20MPa (group C); the HBO treatment group at 0. 22 Mpa ( group D); the HBO treatment group at 0.25 Mpa ( group E). Segments of injured spinal cord were collected from the animals of the 5 groups for studies on the 3rd, 7th, and 14th days after injury. The apoptosis cells were labeled with Tunel and the neurologic function of the spinal cord was assessed in the open field ( the BBB score ). Results The number of Tunel - positive cells decreased considerably and the BBB score improved significantly in all the animals of the HBO groups when compared with those of group A ( P < 0. 05 ). Same results were found when the group C, group D and group E were compared with group B, with statistical significance( P <0. 05). The number of Tunel-positive cells were decreased considerably and the BBB score improved significantly on 3rd and 7th days in group E, when compared with those of group C( P < 0. 05 ), with statistical significance( P < 0. 05 ). However, no statistical significance could be noted on the 14th day (P <0.05). Conclusions HBO could inhibit apoptosis in rats following spinal cord injury, which might be correlated with the increase of pressure within a certain range.  相似文献   

18.
胚胎脊髓不同移植方法促进成鼠损伤脊髓功能恢复的研究   总被引:1,自引:0,他引:1  
目的研究提供血运的胚胎脊髓移植对成鼠损伤脊髓功能恢复的作用。方法将胚胎脊髓组织、胚胎十大网膜组织、胚胎+椎旁肌组织移植到成鼠半切洞损伤的脊髓中,手术后进行联合行为评分,感觉诱发电位,运动诱发电位检查。结果联合行为评分,单纯移植组和胚胎+大网膜组织优于单纯损伤组,感觉诱发电位,运动诱发电位潜峰时的恢复,移植各组均优于单损伤组。胚胎+大网膜组效果最好,单纯胚胎脊髓移植组优于胚胎+椎旁肌移植组。结论通过各种功能检查表明提供血运的胚胎脊髓移植对成鼠损伤脊髓功能恢复有较好的促进作用。  相似文献   

19.
目的:观察人Po-5,flanking介导的21.5ku髓鞘碱性蛋白(myelin basic protiein,MBP)微基因(暂命名为pSVPoMcat)修饰雪旺细胞(SC)在鼠脊髓内存活及其基因表达。方法:120只大鼠分为3组,A组为pSVPoMcat微基因修饰SC移植组;B组为高纯化SC移植组;C组为脊髓损伤(SCI)_对照组,伤后各组分别于2,4,8,12周(每组每次10只),取移植区脊髓切片,进行S-100蛋白,MBP免疫细胞化学染色及地高辛(DIG)标记的hMBPF2 cDNA探针的原位杂交(ISH)测定。结果:伤后2,4,8,12周,A组S-100,MBP染色细胞和ISH细胞差异无统计学意义(P<0.05),其中ISH阳性细胞可见髓鞘形成,B组的S-100染色细胞逐步递减,差异有非常显著性意义(P<0.01),未发现MBP染色细胞以及ISH细胞,C组未发现任何阳性细胞,结论:pSVPoMcat微基因修饰SC在鼠损伤脊髓内能长期存活并表达外源基因,且有助于受伤脊髓的髓鞘形成。  相似文献   

20.
用2.74g和1.03g钢球分别射击10只猪的颈背部,造成软组织贯通伤。位于伤道外的脊髓(10只)、脑(10只)、心脏(9只)和肺(3只)见到出血和肺大泡(1只),其中2.74g组伤情较1.03g组更为严重。2只实验猪分别于伤后3和5min死于严重的脑脊髓震荡伤(脊髓休克)。分析了颈部贯通伤远达效应病变特点:脑脊髓致伤机率增加,脑脊髓出血波及范围广泛,出血病变呈跳跃式分布,预后较差,多见早期死亡。前颅腔内压力峰值可达到1300~1810kPa,其压力值与邻近的颈后部软组织内压力值(1600~1810kPa)接近。认为颈部椎管外贯通伤时,伤道外脑脊髓病变的致伤机理主要是压力波和瞬时空腔作用的结果,但作用途径有差别。  相似文献   

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