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目的建立3种小鼠失血性休克模型,比较血压、血气、血细胞计数等指标,为失血性休克相关实验动物模型的选择提供依据。方法将32只雄性BALA/C小鼠随机均分为失血30%控量组(V1组)、失血40%控量组(V2组)、35-40 mm Hg控压组(P组)和对照组(Control组),通过股动脉插管放血制作失血性休克模型,连续监测血压,90 min时取动脉血进行血气分析和血细胞计数。结果 Control、P组平均动脉压保持稳定,分别为(90.4±1.2)mmHg、(37.8±1.0)mm Hg,血压波动性分别为(3.05±0.16)%、(2.64±0.23)%;V1、V2组平均动脉压均在放血完毕后5 min左右进入平台期,分别为(64.0±2.9)mm Hg、(47.2±3.4)mm Hg,血压波动性分别为(13.66±2.29)%、(16.57±3.01)%;血气检测结果中Control、V1、V2、P组相比较,Hb(g/d L)为14.9±0.7、11.9±0.4、11.2±0.3和10.4±0.6(P<0.01),Hct(%)为45.5±2.1、36.5±1.2、34.4±1.0和32.0±1.6(P<0.01),Lac(mmol/L)为3.6±0.8、2.4±0.4、3.6±0.3和5.0±1.1(P<0.01),K+(mmol/L)为4.2±0.3、4.0±0.3、5.0±0.2和5.6±0.8(P<0.01);血细胞计数结果中Control、V1、V2、P组相比较,RBC(10×12/L)为10.58±0.55、8.84±0.42、8.39±0.46和7.71±0.54(P<0.01),WBC(10×9/L)为8.24±2.54、4.32±1.06、3.57±0.75和4.12±0.80(P<0.01),Plt(10×9/L)为724±80、661±103、577±66和607±94(P>0.05)。结论失血30%、40%控量组血流动力学变化过程接近临床,适于失血性休克后代谢情况、病理生理、存活情况及治疗策略的研究。35-40 mm Hg控压组休克程度重、血压波动性较小,适于失血性休克后代谢性酸碱平衡紊乱、药效学、器官损伤及其分子机制的研究。
Objective To establish three models of hemorrhagic shock in mice and compare indexes such as blood pressure, blood gas, blood cell count and so on to provide the basis for the choice of experimental animal model of hemorrhagic shock. Methods Thirty-two male BALB / c mice were randomly divided into 30% blood loss control group (V1), 40% blood loss control group (V2), 35-40 mm Hg control group (P) and control Group (Control group). The model of hemorrhagic shock was established by cannulation of femoral artery. Blood pressure was monitored continuously and arterial blood was collected at 90 min for blood gas analysis and blood cell count. Results The mean arterial pressure of Control and P groups remained stable at (90.4 ± 1.2) mmHg and (37.8 ± 1.0) mmHg respectively, and the blood pressure variability was 3.05 ± 0.16% and 2.64 ± 0.23% respectively. V1 and V2 The average arterial pressure in the group reached plateau at about 5 min after the completion of exsanguination, and were (64.0 ± 2.9) mm Hg and (47.2 ± 3.4) mm Hg respectively. The blood pressure fluctuations were (13.66 ± 2.29)% and (16.57 ± 3.01) )%; Hb (g / d L) was 14.9 ± 0.7, 11.9 ± 0.4, 11.2 ± 0.3 and 10.4 ± 0.6 (P <0.01) ) Were 45.5 ± 2.1, 36.5 ± 1.2, 34.4 ± 1.0, and 32.0 ± 1.6 (P <0.01) with Lacs of 3.6 ± 0.8, 2.4 ± 0.4, 3.6 ± 0.3 and 5.0 ± 1.1 (P <0.01) , K + (mmol / L) were 4.2 ± 0.3, 4.0 ± 0.3, 5.0 ± 0.2 and 5.6 ± 0.8 respectively (P <0.01) L) were 10.58 ± 0.55,8.84 ± 0.42,8.39 ± 0.46 and 7.71 ± 0.54 (P <0.01), WBC (10 × 9 / L) were 8.24 ± 2.54, 4.32 ± 1.06, 3.57 ± 0.75 and 4.12 ± 0.80 <0.01), Plt (10 × 9 / L) was 724 ± 80, 661 ± 103, 577 ± 66 and 607 ± 94 (P> 0.05). Conclusions The hemodynamic changes in 30% and 40% control groups are close to clinical and suitable for the study of metabolic status, pathophysiology, survival and therapeutic strategies after hemorrhagic shock. The 35-40 mm Hg control group had severe shock and low blood pressure fluctuation, which was suitable for the metabolic acid-base balance disorder, pharmacodynamics and organ damage after hemorrhagic shock and its molecular mechanism.