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百草枯是什么? Paraquat poisoning

[日期:2008-11-09]   [字体: ]

百草枯中毒
  【概述】
  百草枯,称为百草枯肺(paraquet lung)(1.1’二甲基-4.4’二氯二吡啶1.1’-dimethyl-4.4’-dipyridiumdichloride)是一种强烈的杀灭杂草的除莠剂,对人、畜有很强的毒性作用。大多数由于误服或自杀口服引起中毒,但也可经皮肤吸收中毒致死。
  【临床表现】
  摄入除莠剂,可引起舌、口及咽部烧灼感,发生食管炎和胃炎,致呕吐和腹痛。药物从肾脏排泄可损害肾小管,产生蛋白尿、血尿,血中尿素氮、肌酐升高等肾功能损害的表现。呼吸系统主要表现为进行性呼吸困难和紫绀,最终导致呼吸衰竭而死亡。胸部X线表现:最初呈散在的细斑点状阴影,以下肺野较多。迅速进展,病灶融合呈严重的肺水肿样形态。肺功能主要表现为一氧化碳弥散障碍、中等度气道阻塞和(或)限制性通气异常。心、肝及肾上腺中毒可引起相应的症状和体征。
  【病理说明】
  百草枯口服后吸收快,主要蓄积在肺和肌肉中,排泄缓慢,因此毒性作用可持续存在。病变主要发生于肺,称为百草枯肺(paraquet lung)。除莠剂能产生过氧化物离子(O-2)损害I型和Ⅱ型肺泡上皮细胞,引起肿胀、变性和坏死,抑制肺表面活性物质的产生。基本病变为增殖性细支气管炎和肺泡炎。肺的形态学变化取决于摄入后生存期的长短。在1周内死亡者,示肺充血、水肿,肺脏重量增加,类似于氧中毒。生存期超过1周者,肺泡渗出物(含脱落的肺泡上皮碎屑、巨噬细胞、红细胞及透明膜)机化、单核细胞浸润、出血和间质成纤维细胞增生、肺泡间质增厚,其结果发生广泛的纤维化,形成蜂窝状肺及细支气管扩张。百草枯中毒可引起肾小管坏死,肝中央小叶细胞损害、坏死、心肌炎、肺动脉中层增厚,肾上腺皮质坏死等。
  【治疗说明】
  治疗原则是减少毒物的吸收、促进体内毒物排泄、加强支持治疗。首先用矽酸铝(bentonite),或漂布土(Fuller′s earth)或经胃管每2小时给活性炭60克作胃肠灌洗;继可用血液灌流吸附毒物往往能挽救重危患者。有作者用过氧化物岐化酶(superoxidedismutase)预防氧离子形成,或用大剂量VitE作抗氧化剂疗法,但其疗效尚未肯定。由于高浓度氧吸入能增强百草枯的毒性作用,故氧疗时,氧浓度不宜过高,使动脉血氧分压达到70mmHg即可。在慢性中毒的患者,通常给予大剂量皮质类固醇,可减轻症状,但对病理变化改善不明显。呼吸困难者应及时作人工辅助呼吸。急性中毒者,血浆中百枯草水平与生存率有一定关系,若在摄入后6、8、24小时血液中除莠剂浓度超过2、1.2和0.2mg/L,则难以存活。国外报道本病死亡率约33%~50%。 百草枯中毒后千万不可吸氧,会加重病情。
  百草枯中毒的解救方法:
  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。因其毒性大,目前国外已很少应用,国内仍在广泛应用。其产品为20%~50%的水溶液,可经皮肤、呼吸道、消化道进入体内。人类主经经口服吸收中毒,致死量为10~5毫升。一般中毒后5天左右,即可出现口腔和食道溃疡。中毒后5~8天,可出现发热、心率加快、呼吸急促或呼吸衰竭。口服30mg/kg以上,可在48小时出现肺水肿及咯血等呼吸道症状。肺纤维化所致呼吸循环衰竭是致死的主要原因。其病死率很高,约在90%以上。
  误服除草剂百草枯后,一定要尽早抢救
  
  1.尽早充分洗胃,加速排泄。
  目前尚无百草枯中毒的有效解毒剂。鉴于百草枯在胃肠道的吸收率仅为5%~15%,且在酸性及中性环境中稳定,可在碱性溶液中水解。所以,抢救时应尽早使用碱性液体充分洗胃,如应用活性炭加柠檬酸洗胃。为了加速排泄,可用硫酸镁、甘酸醇、大黄等。
  2.尽早应用保肺药物。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。因此,应尽早使用超氧化物歧化酶(SOD)及百草枯单克隆抗体、大剂量维生素C和E,以防止氧自由基形成过多过快,减轻其对细胞膜结构的破坏。
  3.尽早使用呼吸机。以增加气体交换,改善氧合功能,提高氧分压,减轻肺损伤。
  4.尽早进行血液灌流。有经验证明,未灌流患者生存时间超过48小时者均出现了肺、肝、胃的严重损害,最终死于多器官功能衰竭。

Paraquat poisoning
】 【Overview
Paraquat, known as pulmonary paraquat (paraquet lung) (1.1 'dimethyl -4.4' dichloride pyridine 1.1 '-dimethyl-4.4'-dipyridiumdichloride) is a strong kill the weed herbicides, , A strong animal toxicity. As the majority of suicide or wrongly oral poisoning, but can also be absorbed by the skin of poisoning to death.
【Clinical】
Intake of herbicides, which can cause the tongue, mouth and throat burning, the occurrence of esophagitis and gastritis, induced vomiting and abdominal pain. Drug can be excreted from the kidney tubular damage, resulting in proteinuria, hematuria, blood urea nitrogen, creatinine, and other higher Renal damage. Respiratory mainly proGREssive dyspnea and cyanosis, leading to respiratory failure and death. Chest X-ray findings: the first was scattered in the small dot-like shadow, following lung field more. The rapid progress of integration lesions were serious pulmonary edema-like shape. The main function for the performance of the carbon monoxide diffusion barriers, medium degree of airway obstruction and (or) restrictive ventilation abnormalities. Heart, liver and adrenal gland can be caused by the poisoning symptoms and signs.
Note】 【pathology
After the rapid oral absorption of paraquat, the main stock in the lung and muscle, slow excretion, the toxicity of sustainable existence. The main changes took place in the lungs, called pulmonary paraquat (paraquet lung). Herbicides can produce peroxide ions (O-2) damage and I-Ⅱ alveolar epithelial cells, causing swelling, degeneration and necrosis, inhibit pulmonary surfactant production. Essential for the proliferation of disease bronchiolitis and alveolitis. The morphological changes in the lung after the intake depends on the length of survival. 1 week in the death, said congestive heart lung, edema, increased lung weight, similar to oxygen poisoning. Survival over 1 week, alveolar exudate (including loss of alveolar epithelial debris, macrophages, red blood cell membrane and transparent) machine, monocyte infiltration, hemorrhage and interstitial fibroblasts proliferation by alveolar interstitial Thick, the result of extensive fibrosis, the formation of honeycomb lung and small bronchiectasis. Paraquat poisoning can cause renal tubular necrosis, the central lobular liver cell damage, necrosis, myocarditis, pulmonary artery thickening middle, the adrenal cortex, such as necrosis.
Note】 【treatment
The principle of treatment is to reduce the absorption of the poison, and promote excretion of toxins in the body, to strengthen support for treatment. First of all, with aluminum silicate (bentonite), or cloth bleaching earth (Fuller's earth) or gastric tube every 2 hours to 60 grams of activated carbon for gastrointestinal lavage; hemoperfusion adsorption can be used following the poison can often save critically ill patients. The author has used peroxide SOD (superoxidedismutase) to prevent the formation of oxygen ions, or high-dose antioxidant therapy for VitE, but its efficacy has not yet sure. Due to the high concentration of oxygen inhalation can enhance the toxicity of paraquat, the oxygen, the oxygen concentration should not be too high so that the arterial partial pressure of oxygen can be reached 70mmHg. In patients with chronic poisoning is usually given to high-dose corticosteroids can reduce symptoms, but it was not obvious to improve the pathological changes. Breathing difficulties should be assisted in time for artificial respiration. Acute poisoning, plasma subtilis cent survival rate and the level of a certain relationship, if the intake 6,8,24 hours after the blood concentration of herbicides and 2,1.2 more than 0.2mg / L, it is difficult to survive. Foreign reports of the disease mortality by about 33% to 50%. Paraquat poisoning after tens of millions of non-oxygen, will add to the illness.
Paraquat poisoning of relief:
Paraquat, also known as Gramoxone, is a class of heterocyclic organic pesticides, is the world's earlier application of herbicides. Because of their toxicity, at present there are only a few applications of foreign and domestic are still widely used. Its products is 20% to 50% of the solution, by the skin, respiratory tract, gastrointestinal tract into the body. As the main human oral absorption by poisoning, lethal dose of 10 to 5 milliliters. General poisoning after 5 days or so, can appear in oral and esophageal ulcers. After the poisoning 5 to 8 days, fever, speed up the heart rate, shortness of breath or respiratory failure. 30mg/kg oral more than 48 hours may appear pulmonary edema and respiratory symptoms such as hemoptysis. Pulmonary fibrosis caused by respiratory and circulatory failure is the main cause of death. Its high fatality rate, about 90%.
Herbicide paraquat wrongly, as soon as possible to rescue

1. Gastric lavage full as soon as possible to speed up discharge.
Paraquat poisoning is no effective antidote. In view of the paraquat in the gastrointestinal absorption rate of only 5% to 15%, and in acidic and neutral environment of stability, can be hydrolyzed in alkaline solution. Therefore, when the rescue as soon as possible the use of alkaline liquid full gastric lavage, such as the application of activated carbon plus citric acid gastric lavage. In order to speed up excretion, magnesium sulfate can be used, Gansuan alcohol, such as rhubarb.
2. Bao pulmonary drug application as soon as possible. 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. As a result, as soon as possible the use of superoxide dismutase (SOD) and paraquat monoclonal antibody, high-dose vitamin C and E, in order to prevent the formation of oxygen free radicals too much too fast, reducing its impact on the structure of the cell membrane damage.
3. Ventilator use as soon as possible. To increase the gas exchange, to improve oxygenation and enhance the partial pressure of oxygen and reduce lung injury.
4. Hemoperfusion as soon as possible. Experience has shown that there is no time for the survival of patients with reperfusion more than 48 hours there have been both lungs, liver and stomach damage and eventually died of multiple organ failure.
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