The evaluation of the cardiovascular toxicity of surfactants contained in agricultural chemicals

农用化学品中表面活性剂的心血管毒性评价

基本信息

  • 批准号:
    07672455
  • 负责人:
  • 金额:
    $ 1.34万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    1995
  • 资助国家:
    日本
  • 起止时间:
    1995 至 1997
  • 项目状态:
    已结题

项目摘要

A herbicide Basta (BST), containing glufosinate ammonium (GLA), an anionic surfactant (AES), and a glycol (GLY), causes circulatory failre with a decrease in vasculr resistance in human oral poisoning. We tried to elucidate the exact component that is mostly responsible for the cardiovascular effects of this herbicide formulation. In isolated right atria beating spontaneously in Krebs-Ringer's solusion, BST and AES produced negative chronotropic responses in a concentration dependent manner. In electrically driven isolatred left atria, BST and AES caused positive intoropic responses concentration dependently but negative inotropic responses at extremely high concentrations. In aortic segments, BST and AES produced significant vasodilative effects when the aorta was precontracted with phenylephrine. In anesthetized rats, low doses of BST and AES produced a decrease in blood pressure with a slight increase in heart rate, which was suspected to the baroreflex induced by the decrease in blood pressure. At an extremely high dose, BST and AES produced a decrease in blood pressure with a marked decrease in heart rate. The changes induced by BST and AES both in in vitro and in vivo experiments occrred to a similar degree. On the other hand, GLA and GLY did not produce sigmificant effects in either in vitro or in vivo experiments. We conclude that the direct cariovasular effects of BST are mostly caused by the surfactant AES through its vasodilative effects plus cardiostimulative effects at low doses and cardiosuppressive effects at high doses.
除草剂Basta(BST)含有草铵膦铵(GLA)、阴离子表面活性剂(AES)和乙二醇(GLY),在人类口服中毒中会导致循环衰竭,血管抵抗力下降。我们试图阐明确切的组成部分,主要是负责心血管的影响,这种除草剂配方。在Krebs-Ringer液中的离体右心房自发搏动中,BST和AES均产生浓度依赖性的负性变时性反应。在电驱动的离体左心房,BST和AES浓度依赖性地引起正性内视反应,但在极高浓度下引起负性变力反应。在主动脉节段,BST和AES产生显着的血管舒张作用时,主动脉预收缩与苯丙氨酸。在麻醉大鼠中,低剂量BST和AES引起血压下降,心率略有增加,这可能是血压下降引起的压力感受性反射。在极高的剂量下,BST和AES使血压降低,心率明显降低。BST和AES在体外和体内实验中引起的变化程度相似。另一方面,GLA和GLY在体外或体内实验中均不产生显著的作用。我们得出结论,BST的直接心血管效应主要是由表面活性剂AES通过其血管舒张作用加上低剂量的心脏刺激作用和高剂量的心脏抑制作用引起的。

项目成果

期刊论文数量(11)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Kanji Koyama, Kyoko Koyama Katsutoshi Goto.: "Cardiovascular Effects of a Herbicide Containing Glufosinte and a Surfactant : In Vitro and in Vivo Analvis in Rats." Toxicology and Applied Pharmacology. 145. 409-414 (1997)
Kanji Koyama、Kyoko Koyama Katsutoshi Goto.:“含有草铵膦和表面活性剂的除草剂对心血管的影响:大鼠体外和体内肛门”。
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  • 影响因子:
    0
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  • 通讯作者:
Kanji Koyama, Yoshitoshi Kasuya, Kyoko Koyama, Katsutoshi Goto.: "Nitric Oxicide-Mediated Vasorelaxation Induced by Sodium Plyoxuethylene Laurylether Sulfate." Toxicology and Applied Pharmacology. 145. 294-300 (1997)
Kanji Koyama、Yoshitoshi Kasuya、Kyoko Koyama、Katsutoshi Goto.:“聚氧乙烯十二烷基醚硫酸钠诱导的一氧化氮介导的血管舒张。”
  • DOI:
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    0
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  • 通讯作者:
Kanji.Koyama, Yoshitoshi.Kasuya, Kyoko.Koyama, Katsutoshi.Goto: "Nitric Oxicide-Mediated Vasorelaxation Induced by Sodium Plyoxuethylene Laurylether Sulfate." Toxicology and Applied Pharmacology. 145. 294-300 (1997)
Kanji.Koyama,Yoshitoshi.Kasuya,Kyoko.Koyama,Katsutoshi.Goto:“聚氧乙烯十二烷基醚硫酸钠诱导的一氧化氮介导的血管舒张。”
  • DOI:
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  • 影响因子:
    0
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小山 完二: "グルホシネートを主成分とする除草剤による中毒" 医学のあゆみ. 185. 192-193 (1998)
Kanji Koyama:“以草铵膦为主要成分的除草剂中毒”《医学史》185. 192-193 (1998)。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Kanji.Koyama: ""Agricultural chemicals"in Oxford Textbook of Critical Care" Oxford University Press(in press), (1998)
小山宽治:《牛津重症监护教科书中的“农业化学品”》牛津大学出版社(正在出版),(1998)
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  • 影响因子:
    0
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KOYAMA Kanji其他文献

KOYAMA Kanji的其他文献

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{{ truncateString('KOYAMA Kanji', 18)}}的其他基金

The Relationship between Serum Glufosinate Concentration and Severity of Poisoning Caused by the Ingestion of a Herbicide Containing Glufosin
草铵膦血清浓度与摄入含草铵膦除草剂中毒严重程度的关系
  • 批准号:
    10672144
  • 财政年份:
    1998
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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