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[活性炭对口服百草枯中毒吸附效果的评估:大型动物实验研究]

[Evaluation of adsorption effect of activated charcoal on oral paraquat poisoning: an experimental study on large animal].

作者信息

Sun Baisheng, He Yuezhong, Pei Yuhao, Zhang Cong, Zhang Xigang, Yang Zhan

机构信息

Department of Emergency, Affiliated Hospital of Academy of Military Medical Sciences, Beijing 100071, China (Sun BS, Pei YH, Zhang C, Zhang XG, Yang Z); Department of Science and Technology, Academy of Military Medical Sciences, Beijing 100850, China (He YZ). Corresponding author: He Yuezhong, Email:

出版信息

Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2017 Mar;29(3):211-215. doi: 10.3760/cma.j.issn.2095-4352.2017.03.004.

Abstract

OBJECTIVE

To study the adsorption effect of activated charcoal suspension on paraquat (PQ) in gastrointestinal tract of beagles exposed to PQ.

METHODS

Twenty healthy male beagles were randomly divided into experimental group and control group, with 6 beagles in each group. 20% PQ solution (a dose of 30 mg/kg) was prescribed through stomach for beagles in both groups. After exposure to PQ for 30 minutes, the beagles in experimental group were given activated charcoal suspension (1.0 g/kg of type I activated charcoal powder mixed with 100 mL of normal saline) by gavage, while the control group was only given equal volume of normal saline. After exposure to PQ for 10 minutes, 30 minutes, and 1, 2, 4, 8, 12, 24, and 48 hours, blood was collected from hepatic portal veins and peripheral veins to detect the PQ concentration change in the plasma. The toxicokinetics software DAS 2.1.1 was applied to analyze PQ concentration and compare the change in toxicokinetics parameters between the both groups. The change in vital signs including heart rate (HR), respiratory rate (RR) and pulse oxygen saturation (SpO) was dynamically monitored 10 minutes before exposure, 4 hours and each day from the 1st to the 7th day after exposure.

RESULTS

After exposure to PQ, the poison concentration in the plasma of hepatic portal veins and peripheral veins in the control group rose quickly and reached peak 4 hours later. It fell quickly at first, and fell slowly 8 hours later. But in the experimental group, the increase rate to the peak was significantly slow. Besides, PQ peak fell more obviously than that in the control group and it was about 50% of the control group (μg/L: 123.50±11.67 vs. 255.18±12.29 in blood from hepatic portal veins, 122.35±11.72 vs. 250.86±11.15 in blood from peripheral veins). After 8 hours it fell much more quickly than that of the control group. After exposure to PQ for 48 hours, PQ concentration in the plasma was still lower than that of the control group (μg/L: 0.53±0.18 vs. 15.98±5.58 in blood from hepatic portal veins, 0.31±0.01 vs. 15.03±4.82 in blood from peripheral veins, both P < 0.01). With the toxicokinetics analysis, compared with the control group, the maximum concentration (Cmax) and area under the curve (AUC) of PQ in the plasma of hepatic portal veins and peripheral veins in the experimental group were significantly decreased [Cmax (μg/L): 125.07±9.49 vs. 255.18±12.29 in blood from hepatic portal veins, 123.38±9.52 vs. 250.86±11.15 in blood from peripheral veins; AUC (mg×L×h): 1.6±0.2 vs. 3.3±0.4 in blood from hepatic portal veins, 1.5±0.2 vs. 3.2±0.3 in blood from peripheral veins], time to the peak (Tmax) of PQ was slowed (hours: 5.3±1.9 vs. 4.0±0.0 in blood from hepatic portal veins, 4.7±1.5 vs. 4.0±0.0 in blood from peripheral veins), and PQ plasma half-life (t) and mean retention time (MRT) were significantly shortened [t (hours): 3.8±1.2 vs. 15.4±3.7 in blood from hepatic portal veins, 3.5±1.0 vs. 15.5±2.7 in blood from peripheral veins; MRT (hours): 8.0±1.5 vs. 13.4±1.2 in blood from hepatic portal veins, 7.6±1.3 vs. 13.3±1.2 in blood from peripheral veins; all P < 0.01]. After exposure to PQ, HR and RR in both the experimental group and the control group increased and reached to the peak about the 4th day and then the increase rate began to slow down gradually; SpO slowed down gradually and reached to the valley about the 4th day and then it began to recover, but the change range of vital signs in the experimental group was smaller than that of the control group, and the parameters were significantly better than those of control group [4-day HR (bpm): 134.50±3.04 vs. 142.00±6.43, 4-day RR (times/min): 31.00±0.58 vs. 34.33±0.94, 4-day SpO: 0.900±0.006 vs. 0.873±0.005, all P < 0.05].

CONCLUSIONS

Activated charcoal administrated at 30 minutes after PQ poisoning can slow down the increase rate of PQ concentration in the plasma, decrease the peak concentration and has less influence on vital signs in beagles.

摘要

目的

研究活性炭混悬液对百草枯(PQ)中毒比格犬胃肠道内PQ的吸附作用。

方法

将20只健康雄性比格犬随机分为实验组和对照组,每组6只。两组比格犬均经胃给予20% PQ溶液(剂量为30 mg/kg)。PQ染毒30分钟后,实验组比格犬经口灌胃给予活性炭混悬液(1.0 g/kg I型活性炭粉与100 mL生理盐水混合),对照组仅给予等体积生理盐水。PQ染毒10分钟、30分钟以及1、2、4、8、12、24和48小时后,从肝门静脉和外周静脉采集血液,检测血浆中PQ浓度变化。应用毒代动力学软件DAS 2.1.1分析PQ浓度,并比较两组毒代动力学参数的变化。在染毒前10分钟、染毒后4小时以及染毒后第1天至第7天每天动态监测包括心率(HR)、呼吸频率(RR)和脉搏血氧饱和度(SpO)在内的生命体征变化。

结果

PQ染毒后,对照组肝门静脉和外周静脉血浆中毒物浓度迅速升高,4小时后达到峰值。起初下降迅速,8小时后下降缓慢。但实验组达到峰值的上升速率明显减慢。此外,PQ峰值下降比对照组更明显,约为对照组的50%(肝门静脉血中μg/L:123.50±11.67 vs. 255.18±12.29,外周静脉血中122.35±11.72 vs. 250.86±11.15)。8小时后下降比对照组快得多。PQ染毒48小时后,血浆中PQ浓度仍低于对照组(肝门静脉血中μg/L:0.53±0.18 vs. 15.98±5.58,外周静脉血中0.31±0.01 vs. 15.03±4.82,均P < 0.01)。经毒代动力学分析,与对照组相比,实验组肝门静脉和外周静脉血浆中PQ的最大浓度(Cmax)和曲线下面积(AUC)显著降低[Cmax(μg/L):肝门静脉血中125.07±9.49 vs. 255.18±12.29,外周静脉血中123.38±9.52 vs. 250.86±11.15;AUC(mg×L×h):肝门静脉血中1.6±0.2 vs. 3.3±0.4,外周静脉血中1.5±0.2 vs. 3.2±0.3],PQ达峰时间(Tmax)延迟(小时:肝门静脉血中5.3±1.9 vs. 4.0±0.0,外周静脉血中4.7±1.5 vs. 4.0±0.0),且PQ血浆半衰期(t)和平均滞留时间(MRT)显著缩短[t(小时):肝门静脉血中3.8±1.2 vs. 15.4±3.7,外周静脉血中3.5±1.0 vs. 15.5±2.7;MRT(小时):肝门静脉血中8.0±1.5 vs. 13.4±1.2,外周静脉血中7.6±1.3 vs. 13.3±1.2;均P < 0.01]。PQ染毒后,实验组和对照组的HR和RR均升高,约在第4天达到峰值,随后升高速率逐渐减慢;SpO逐渐减慢,约在第4天达到谷底,随后开始恢复,但实验组生命体征的变化幅度小于对照组,且各项参数均显著优于对照组[第4天HR(次/分钟):134.50±3.04 vs. 142.00±6.43,第4天RR(次/分钟):31.00±0.58 vs. 34.33±0.94,第4天SpO:0.900±0.006 vs. 0.873±0.005,均P < 0.05]。

结论

PQ中毒后30分钟给予活性炭可减慢血浆中PQ浓度的上升速率,降低峰值浓度,且对比格犬生命体征影响较小。

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