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目的:探讨低温暴露对创伤性休克复苏后大鼠炎性因子表达的影响。方法:72只SD雄性大鼠(300~350g)随机分为常温假手术组(常假组)、低温假手术组(低假组)、常温创伤性休克组(常创组)、低温创伤性休克组(低创组),每组18只大鼠。动物称重后水合氯醛腹腔注射麻醉,创伤性休克组采用股骨创伤骨折并放血法制作创伤性休克模型,假手术组只行双侧颈动、静脉插管。复苏后将各组大鼠置于相应的温度下观察,记录各组的肛温,各组分别在8、24、36h时间点处死6只大鼠,用ELISA试剂盒检测各组血清和心肺中IL-6、TNF-α、IL-1β、IL-10的浓度。结果:低创组置于低温环境后,体温短暂降低,6h左右逐渐上升,0~8h维持在28℃~35℃的亚低温状态,16h后维持在37℃~38℃的恒温水平。在8h时,低创组血清、心肺组织中炎性因子IL-6、TNF-α和IL-1β表达水平明显低于常创组(P<0.05),IL-10表达水平明显高于常创组(P<0.05);而在36h时,低创组血清和心肺组织中炎性因子IL-6、TNF-α和IL-1β表达水平明显高于常创组(P<0.05),IL-10表达水平明显低于常创组(P<0.05)。结论:低温暴露早期能显著改善创伤性休克复苏后大鼠的血清和心肺组织的炎症反应,而晚期则会加剧血清和心肺组织的炎症反应,可能会对心肺组织造成更大的损伤。
Objective: To investigate the effect of hypothermic exposure on the expression of inflammatory cytokines in rats after traumatic shock resuscitation. Methods: Seventy-two SD male rats (300-350g) were randomly divided into two groups: normal control group (normotensive group), hypothermia group (normotensive group), traumatic shock group Shock group (low-invasive group), each group of 18 rats. The animals were anesthetized by intraperitoneal injection of chloral hydrate after trauma. Traumatic shock group was treated by traumatic fracture of femur and traumatic shock model was made by exsanguination. Sham operation group received bilateral carotid and venous cannula only. After resuscitation, the rats in each group were placed under the corresponding temperature and the rectal temperature of each group was recorded. Six rats were sacrificed at 8, 24, and 36 hours respectively. Serum and heart and lung IL-6, TNF-α, IL-1β, IL-10. Results: After being placed in the low temperature environment, the body temperature decreased briefly and gradually increased at 6h, maintained at 28 ℃ ~ 35 ℃ in 0 ~ 8h and maintained at 37 ℃ ~ 38 ℃ after 16h. At 8h, the expression levels of IL-6, TNF-α and IL-1βin the low-invasive group were significantly lower than those in the untreated group (P <0.05), and the levels of IL-10 were significantly higher than those in the non-invasive group (P <0.05). At 36h, the expression of IL-6, TNF-α and IL-1βin serum and cardiopulmonary tissues of low-invasive group were significantly higher than those in the untreated group (P <0.05) 10 expression level was significantly lower than the conventional group (P <0.05). CONCLUSION: Early low-temperature exposure can significantly improve the inflammatory response of serum and cardiopulmonary tissue in rats after traumatic shock and resuscitation, while the late phase may exacerbate inflammatory reaction in serum and cardiopulmonary tissue, which may cause more damage to heart and lung tissue.