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甲基泼尼松龙与血管平滑肌中的肾上腺素能机制

Methylprednisolone and adrenergic mechanisms in vascular smooth muscle.

作者信息

Bengtsson B

出版信息

Acta Physiol Scand. 1981 Jun;112(2):129-36. doi: 10.1111/j.1748-1716.1981.tb06795.x.

Abstract

The influence of methylprednisolone on noradrenaline-induced contractions and 3H-noradrenaline release was investigated in isolated preparations of rat aorta and portal vein. 20-200 micro M of methylprednisolone had a slight inhibitory effect on the contractions of the aorta but had no effect in the portal vein. The EC50-values noradrenaline were about 10-6 M in both vessels; methylprednisolone did not change it. The steroid changed neither spontaneous nor potassium (127 mM) induced release of 3H-noradrenaline. The potassium (127 mM) induced contracture in the portal vein had 2 phases; the second, at least partly, was produced by released intramural noradrenaline as it was depressed by reserpinization of the animal. Injection of methylprednisolone to the animal 2 h before sacrifice induced a better maintained second phase of the potassium contracture in the portal vein. Although this could mean the release of increased amounts of noradrenaline, other explanations are also possible.

摘要

在大鼠主动脉和门静脉的离体标本中研究了甲泼尼龙对去甲肾上腺素诱导的收缩和3H-去甲肾上腺素释放的影响。20 - 200微摩尔的甲泼尼龙对主动脉收缩有轻微抑制作用,但对门静脉无影响。去甲肾上腺素在两种血管中的EC50值约为10-6摩尔;甲泼尼龙未改变该值。该类固醇既不改变3H-去甲肾上腺素的自发释放,也不改变钾(127毫摩尔)诱导的释放。钾(127毫摩尔)诱导的门静脉挛缩有两个阶段;第二个阶段至少部分是由壁内释放的去甲肾上腺素引起的,因为动物经利血平化后该阶段受到抑制。在处死动物前2小时给动物注射甲泼尼龙可使门静脉钾挛缩的第二阶段维持得更好。虽然这可能意味着释放了更多的去甲肾上腺素,但也可能有其他解释。

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