Effect of free radicals on pulmonary vascular response to acetylcholine.
Effect of free radicals on pulmonary vascular response to acetylcholine.
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DOI：
10.1152/jappl.1991.71.3.821
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发表时间：
1991-09
影响因子：
3.3
通讯作者：
X. Chen;C. Gillis
中科院分区：
文献类型：
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作者：
X. Chen;C. Gillis
我们描述了一种由电解产生的自由基引起的肺内皮损伤模型。在37 ℃下用含有30 μ M吲哚美辛的Krebs溶液原位灌注兔肺。用20 mA的恒定DC电流电解该溶液2 min，在电流通过期间引起肺血管收缩，并将随后的乙酰胆碱诱导的血管舒张转化为血管收缩。电解也抑制内皮依赖性血管舒张由于钙离子载体A23187，但不是由于硝普钠，这表明平滑肌功能是不变的，而肺的内皮细胞是专门修改的刺激。超氧化物歧化酶和过氧化氢酶的混合物或水杨酸钠可在电解后从溶液中去除羟基自由基，从而防止这些影响。电解诱导的内皮损伤是不太明显的功能时，电解应用在再循环的克雷布斯溶液，也许是因为再循环灌注可能会触发释放自由基清除剂或其他保护物质。这项技术提供了一个简单的可重复的模型，研究自由基相关的损伤内皮细胞在完整的肺。
We describe a model of pulmonary endothelial injury caused by electrolysis-generated free radicals. Rabbit lungs were perfused in situ with Krebs solution at 37 degrees C containing 30 microM indomethacin. Electrolysis of this solution for 2 min, with a constant DC current of 20 mA, caused pulmonary vasoconstriction during the passage of current and converted subsequent acetylcholine-induced vasodilation to vasoconstriction. Electrolysis also inhibited endothelial-dependent vasodilation due to the calcium ionophore A23187 but not that due to sodium nitroprusside, suggesting that smooth muscle function was unaltered, while that of the endothelium of the lung is specifically modified by the stimulus. These effects were prevented by a mixture of superoxide dismutase and catalase or by sodium salicylate, which removes hydroxyl radicals from solution after electrolysis. Electrolysis-induced endothelial damage was less functionally obvious when electrolysis was applied during recirculation of Krebs solution, perhaps because recirculating perfusion may trigger release of either free radical scavengers or other protective substances. This technique offers a simple reproducible model to study free radical-related damage of endothelium in the intact lung.