Lung protection against paraquat is calcium dependent.

Lung protection against paraquat is calcium dependent.
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百草枯对肺部的保护作用依赖于钙。

DOI:
10.1152/jappl.1992.72.2.498
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发表时间:
1992
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Taylor,AE
Taylor,AE
中科院分区:
--
文献类型:
--
作者:
Barnard,JW;Womack,WA;Smith,SM;Engerson,TD;Taylor,AE

文献摘要

被引文献

相似文献

用百草枯对离体、灌流和通气的大鼠肺进行攻击(0.01 M),以确定不同钙浓度或钙依赖性酶活性对百草枯诱导的损伤的影响。测量了节段性血管阻力、微血管渗透性(通过毛细血管过滤系数评估)、肺组织氧化型谷胱甘肽和肺百草枯蓄积。暴露于百草枯2.5小时没有增加微血管通透性或肺血管阻力的存在下,无论是正常的细胞外钙或低细胞外钙和偏钒酸钠。暴露于百草枯的肺仅在细胞外钙含量低或加入三氟拉嗪后才受到损伤(通过过滤系数增加进行评估)。这种损伤与氧化型谷胱甘肽水平降低和百草枯积累增加有关,这表明钙的保护作用是通过抑制百草枯积累和维持NADPH。肺血管阻力没有增加与百草枯挑战。
Isolated, perfused, and ventilated rat lungs were challenged by paraquat (0.01 M) in the presence of 2.5 mM Ca2+, 2.5 mM Ca2+ with trifluoperazine (100 microM), 0.025 mM Ca2+, or 0.025 mM Ca2+ with sodium metavanadate (10 microM) to establish the effect of varying calcium concentration or calcium-dependent enzyme activities on injury induced by paraquat. Segmental vascular resistances, microvascular permeability (as assessed by the capillary filtration coefficient), lung tissue oxidized glutathione, and lung paraquat accumulation were measured. Exposure to paraquat for 2.5 h did not increase microvascular permeability or pulmonary vascular resistance in the presence of either normal extracellular calcium or low extracellular calcium and sodium metavanadate. Lungs exposed to paraquat were injured (as assessed by increased filtration coefficient) only in the presence of low extracellular calcium or after trifluoperazine was added. This injury was associated with decreased levels of oxidized glutathione and increased paraquat accumulation, suggesting that calcium's protective effect was both by inhibition of paraquat accumulation and maintenance of NADPH. Pulmonary vascular resistance was not increased with paraquat challenge.