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谢小均, 陶开宇, 唐梦琳, 等. 大鼠体外循环模型的建立及其效果评价[J]. 四川大学学报(医学版), 2012, 43(5): 770-774.
引用本文: 谢小均, 陶开宇, 唐梦琳, 等. 大鼠体外循环模型的建立及其效果评价[J]. 四川大学学报(医学版), 2012, 43(5): 770-774.
XIE Xiao-jun, TAO Kai-yu, TANG Meng-lin, et al. Establishment and Evaluation of Extracorporeal Circulation Model in Rats[J]. Journal of Sichuan University (Medical Sciences), 2012, 43(5): 770-774.
Citation: XIE Xiao-jun, TAO Kai-yu, TANG Meng-lin, et al. Establishment and Evaluation of Extracorporeal Circulation Model in Rats[J]. Journal of Sichuan University (Medical Sciences), 2012, 43(5): 770-774.

大鼠体外循环模型的建立及其效果评价

Establishment and Evaluation of Extracorporeal Circulation Model in Rats

  • 摘要: 目的 探讨大鼠动-静脉体外循环(extracorporeal circulation,ECC)模型是否能模拟临床体外循环造成的特征性炎性反应和器官损伤。 方法 SD大鼠麻醉,右颈总动脉、左股静脉插管建立循环通路后随机分为2组:ECC组大鼠采用右颈总动脉-左股静脉转流2 h,观察2 h;Sham组大鼠插管后仅进行血液稀释而不行旁路循环,观察4 h。实验结束后取标本测定血常规、血浆炎性细胞因子含量、动脉血气、支气管肺泡灌洗液中炎性因子和肺组织含水量;并使用流式细胞术测定循环内皮细胞数量;另取肺组织做HE染色。 结果 ECC后2 h,ECC组大鼠仍能保持正常红细胞数量,而白细胞数量、血浆中肿瘤坏死因子-α(TNF-α)、中性粒细胞弹性蛋白酶(NE)水平、循环内皮细胞数量均高于Sham组(P<0.05)。肺损伤指标显示:ECC组动物肺氧合指数低于300 mmHg(1 mmHg=0.1333 kPa),并低于Sham组(P<0.05),达到临床急性肺损伤诊断标准;而支气管肺泡灌洗液内TNF-α、肺水含量均高于Sham组(P<0.05),肺组织内可见大量炎性细胞浸润,肺泡膜明显增厚。 结论 经右颈总动脉、左股静脉插管能成功建立大鼠ECC模型,该模型影响因素单一,成功率高,仅转流2 h即能诱导出全身炎性反应综合征和炎性相关急性肺损伤,因此适于研究ECC炎性反应对组织器官功能的影响。

     

    Abstract: Objective To establish an extracorporeal circulation (ECC) rat model, and evaluate the inflammatory response and organ injury induced in the model. Methods SD rats were anesthetized and cannulated from right common carotid artery to left femoral vein to establish the bypass of extracorporeal circulation. Then the rats were randomly divided into ECC group and sham group. The rats in ECC group were subjected to extracorporeal circulation for 2 hours and then rest for 2 hours, while the rats in sham group were only observed for 4 hours without extracorporeal circulation. After that, blood routine examination, blood gas analysis, the measurement of pro-inflammatory factors in bronchoalveolar lavage fluid and lung tissue were performed to evaluate the lung injury induced by ECC. Circulating endothelial cells were also calculated by flow cytometry to assess the vascular endothelial injury. Results At 2 hours after ECC, red blood cell counts in both groups kept normal, while leukocyte and neutrophil counts, plasmatic tumor necrosis factor-α level and neutrophil elastase level, circulating endothelial cells in the rats of ECC group were significantly higher than those in sham group. Tumor necrosis factor-α in bronchoalveolar lavage fluid and water content in lung of the ECC rats were also significantly higher, while the oxygenation index was significantly lower. Neutrophil infiltration was also observed in lung tissues with increased thickness of alveolar membrane in ECC group. Conclusion The ECC model established from right common carotid artery to left femoral vein in our study can successfully induce systemic inflammatory response, and acute lung injury associated with inflammation.

     

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