肾上腺素刺激人体内的血栓素并抑制白三烯的合成。

Eicosanoids Pub Date : 1992-01-01
J Alanko, A Riutta, I Mucha, T Kerttula, S Kaukinen, H Vapaatalo, T Metsä-Ketelä, E Seppälä
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引用次数: 0

摘要

儿茶酚胺和其他儿茶酚类化合物对体外人多形核白细胞和全血花生四烯酸代谢的环加氧酶和5-脂加氧酶途径有相反的作用。高水平的肾上腺素,例如在心肌梗塞中发现,与花生四烯酸代谢的调节有关的假设得到了检验。将肾上腺素(每分钟0.1微克/千克,持续45分钟,随后0.2微克/千克,持续15分钟)输注给健康男性志愿者,以模拟心肌梗死时高水平肾上腺素与花生四烯酸代谢之间的关系。肾上腺素输注增加钙离子载体a23187诱导的全血TXB2形成。当自发凝血作为刺激时,效果较小。尿11-脱氢txb2排泄量(体内总血栓素合成指标)增加了两倍。肾上腺素输注降低了a23187刺激的全血中LTB4和LTE4的合成。这些结果表明,高水平的肾上腺素对人体花生四烯酸代谢的环加氧酶和5-脂加氧酶途径的影响是不同的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Adrenaline stimulates thromboxane and inhibits leukotriene synthesis in man.

Catecholamines and other catecholic compounds have opposite effects on the cyclooxygenase and 5-lipoxygenase pathways of arachidonic acid metabolism in human polymorphonuclear leukocytes and whole blood in vitro. The hypothesis that high levels of adrenaline, found e.g. in myocardial infarction, are involved in the regulation of arachidonic acid metabolism was tested. Adrenaline (0.1 micrograms/kg per min for 45 min and thereafter 0.2 micrograms/kg per min for 15 min) was infused to healthy male volunteers to mimic relationships between high levels of adrenaline and arachidonic acid metabolism in myocardial infarction. Adrenaline infusion increased Ca ionophore A23187-induced TXB2 formation in whole blood. The effect was smaller when spontaneous clotting was used as a stimulus. Urinary 11-dehydro-TXB2 excretion, an indicator of total in vivo thromboxane synthesis, increased twofold. Adrenaline infusion decreased both LTB4 and LTE4 synthesis in A23187-stimulated whole blood. These results demonstrate that high levels of adrenaline influence the cyclooxygenase and 5-lipoxygenase pathways of arachidonic acid metabolism differentially in man.

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