CAJ | 학술논문

目的观察不同复温速率及浅低温对兔肢体爆炸伤合并海水浸泡后机体炎症反应的特点.方法复制肢体爆炸伤合并海水浸泡致低体温[(31.0±0.5℃)]模型.成年家兔24只,随机分为4组,每组6只.Ⅰ组复温至(38.0±0.5)℃,复温速率(8.94±0.93)℃/h;Ⅱ组复温至(38.0±0.5)℃,复温速率(3.88±0.22)℃/h;Ⅲ组复温至(38.0±0.5)℃,复温速率(2.18±0.12)℃/h;H组复温至(34～35)℃并维持至实验结束,复温速率(4.49±0.66)℃/h.以调节环境温度及加温输液的方法将体温恢复到目标体温后维持该体温观察6 h.于致伤前(T0)、浸泡降温后(T1)、复温即刻(T2)、复温后3 h(T3)、复温后6 h(T4)共5个时相点检测血清肿瘤坏死因子(TNF-α)、白介素-1β(IL-1β)、白介素-6(IL-6).实验结束后取动物心、肝、肠、肺、肾组织.测定组织匀浆髓过氧化物酶(MPO)活性.结果复温后,Ⅰ组、H组IL-1β、IL-6、TNF-α值较Ⅱ组、Ⅲ组明显升高(P<0.01或P<0.05),其中Ⅰ组升高更为显著.Ⅰ组、H组心、肝、肠、肺、肾组织匀浆中,MPO活性较Ⅱ组、Ⅲ组明显增高(P<0.01或P<0.05),Ⅱ组、Ⅲ组比较差异无统计学意义.结论肢体爆炸伤合并海水浸泡致低体温后,快速复温及维持机体低体温均可导致机体内IL-1β、IL-6、TNF-α水平明显升高,组织中MPO活性明显增高;缓慢复温则可以明显抑制这3种炎症因子的水平及组织中MPO活性.
목적 관찰불동복온속솔급천저온대토지체폭작상합병해수침포후궤체염증반응적특점.방법 복제지체폭작상합병해수침포치저체온[(31.0±0.5℃)]모형.성년가토24지,수궤분위4조,매조6지.Ⅰ조복온지(38.0±0.5)℃,복온속솔(8.94±0.93)℃/h;Ⅱ조복온지(38.0±0.5)℃,복온속솔(3.88±0.22)℃/h;Ⅲ조복온지(38.0±0.5)℃,복온속솔(2.18±0.12)℃/h;H조복온지(34～35)℃병유지지실험결속,복온속솔(4.49±0.66)℃/h.이조절배경온도급가온수액적방법장체온회복도목표체온후유지해체온관찰6 h.우치상전(T0)、침포강온후(T1)、복온즉각(T2)、복온후3 h(T3)、복온후6 h(T4)공5개시상점검측혈청종류배사인자(TNF-α)、백개소-1β(IL-1β)、백개소-6(IL-6).실험결속후취동물심、간、장、폐、신조직.측정조직균장수과양화물매(MPO)활성.결과 복온후,Ⅰ조、H조IL-1β、IL-6、TNF-α치교Ⅱ조、Ⅲ조명현승고(P<0.01혹P<0.05),기중Ⅰ조승고경위현저.Ⅰ조、H조심、간、장、폐、신조직균장중,MPO활성교Ⅱ조、Ⅲ조명현증고(P<0.01혹P<0.05),Ⅱ조、Ⅲ조비교차이무통계학의의.결론 지체폭작상합병해수침포치저체온후,쾌속복온급유지궤체저체온균가도치궤체내IL-1β、IL-6、TNF-α수평명현승고,조직중MPO활성명현증고;완만복온칙가이명현억제저3충염증인자적수평급조직중MPO활성.
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.