结论百草枯属于中等毒性农药。
目前尚无百草枯中毒的有效解毒剂。
百草枯是一种高效能除草剂。
免疫系统是百草枯致肺纤维化加剧的重要因素。
The immune system plays an important role in exacerbating paraquat-induced lung fibrosis.
方法回顾性分析42例百草枯中毒患者的临床资料。
Methods Clinical data of 42 patients with paraquat poisoning was analyzed retrospectively.
给小鼠灌服不同浓度的百草枯溶液，观察小鼠的中毒症状；
Feed the mice with different doses of liquor of paraquat and observe the toxic symptom.
方法：首先，建立大鼠百草枯中毒致肺纤维化的动物模型。
Methods: Erect a paraquat-induced pulmonary fibrosis animal model first.
目的探讨血必净注射液对于治疗急性百草枯中毒的临床效果。
Objective: To approach the treatment of Xuebijing injection on acute paraquat poisoning.
目的探讨CT对百草枯中毒肺损伤的诊断价值和影像学特征。
Objective Discuss the diagnostic value and video character of ct to lung impairment caused by Paraquat poisoning.
方法对83例口服百草枯中毒患者的临床资料进行回顾性分析。
MethodsTo look back and analyse the clinical material of 83 patients poisoned by paraquat per os.
因此，加强急性百草枯中毒的基础和临床研究具有重要的意义。
Therefore, it was great important significance that the basic and clinical research of acute paraquat intoxication was strengthened.
严重的百草枯中毒的特点是多器官功能衰竭，肺是主要的靶器官。
Severe paraquat intoxication is characterized by multiple organ failure, and the lungs are the most important target organs.
结论百草枯染毒大鼠不同脏器组织在不同时间点其毒物含量不同。
Conclusions There were different paraquat content in different organs tissue and time points in paraquat poisoning rats.
抗性稳定性检验表明，大蒜抗百草枯能力在一定时间内能够保持下去。
Stability test showed the ability of resistant paraquat could keep for a long time.
方法对25例急性百草枯中毒住院患者的临床资料进行回顾性分析。
Methods a retrospectively analysis was conducted on the clinical data of the admitted 25 patients with acute paraquat intoxication within the past 5 years.
目的探讨血液灌流治疗急性百草枯中毒（APP）的效果及护理措施。
Objective To explore therapeutic effect of acute paraquat poisoning (APP) by hemoperfusion and seek for the related nursing measures.
该文就近年来关于百草枯所致肺纤维化发生机制的研究进展进行综述。
Recent studies on the pathogenesis of paraquat-induced pulmonary fibrosis are reviewed in this paper.
评估糖皮质激素和环磷酰胺对百草枯所致的肺纤维化患者死亡率的影响。
To assess the effects of glucocorticoid with cyclophosphamide on mortality in patients with paraquat-induced lung fibrosis.
目的探讨口服百草枯中毒患者口腔护理的方法及早期护理的临床意义。
Objective To investigate the clinical significance of early oral care for paraquat-poisoned patients.
目的分析百草枯中毒预后的相关因素，寻求提高生存率的有效治疗方法。
Objective to analyze the relevant factors about paraquat poison prognosis to find effective treatment to improve the survival rate.
百草枯，又名克无踪，是一类有机杂环类农药，是世界上应用较早的除草剂。
Paraquat, also known as Gramoxone, is a class of heterocyclic organic pesticides, is the world's earlier application of herbicides.
百草枯中毒最常见的并发症是肺间质纤维化，并常因此导致肺功能衰竭而死亡。
Paraquat poisoning the most common complications are pulmonary interstitial fibrosis, and often it leads to respiratory failure and death.
方法：回顾分析17例百草枯农药中毒患者的临床资料、诊疗情况及治疗转归。
Methods: Retrospective analysis was used to study the clinical data of 17 cases with parquet intoxication.
比较两组救治的成功率，并总结对百草枯中毒患者的临床治疗及护理有效的方法。
Compare two sets of treatment, and summarizes the success rate of paraquat intoxication of clinical treatment and nursing effective method.
该方法由于可以通过改变醇的种类，合成出含不同烷基取代基的百草枯衍生物。
The method can synthesize paraquat derivatives containing different alkyl substituents by changing the type of ethanol.
百草枯是毒性很强的除草剂之一，其中毒的报道屡见不鲜，但治疗的效果均不佳。
Paraquat is one of virulent herbicides, the reports of paraquat intoxication are seen repeatedly, but the ideal therapies haven t been found up to now.
通过对12例百草枯中毒患者的抢救与护理，总结出血液灌流和综合护理的重要性。
Acrossed to rescue and care the 12 patients with paraquat poisoning, to sum up the important of blood irrigation and synthetical nursing.
目的：探讨百草枯对黑质细胞线粒体呼吸链的影响和导致黑质细胞损害的可能机制。
Aim: to explore the influence of paraquat on cerebral mitochondrial respiratory chain activity and the possible mechanism of paraquat to damage nigral neurons.
本文对百草枯中毒机制和临床治疗进展作一综述，为临床救治百草枯中毒提供依据。
We summarized the mechanism of paraquat intoxication and prospects of clinical treatment so as to provide the evidences for clinical remedies.
百草枯中毒机理主要是在肺内产生氧自由基，破坏肺细胞，导致肺纤维化和呼吸衰竭。
Paraquat poisoning is a major mechanism of oxygen free radicals produced in the lungs, damage to lung cells, leading to respiratory failure and pulmonary fibrosis.
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