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血管活性药物对离体灌注猪耳纤溶酶原激活物释放的可能作用机制。

A possible mechanism of vasoactive agents on plasminogen activator release in isolated perfused pig ears.

作者信息

Nakajima K

出版信息

Thromb Res. 1983 Jan 15;29(2):187-96. doi: 10.1016/0049-3848(83)90140-8.

Abstract

The mechanism of vasoactive agents on plasminogen activator (PA) release was studied in isolated perfused pig ears. In the perfusion with atropine (3 microM)-containing Tyrode's solution, the enhancement of PA release caused by acetylcholine (1.0 micrograms) was completely inhibited; however, increases caused by other potentiators, namely, bradykinin (1.0 micrograms), histamine (1.0 micrograms), dilazep (30 micrograms), and thrombin (6 U) were not affected. In the case of mepyramine (10 microM), the increase of PA release caused by histamine (1.0 micrograms) was completely inhibited; and that caused by dilazep (30 micrograms) was partially inhibited, however, increases caused by acetylcholine, bradykinin, and thrombin were not influenced. Papaverine (30 microM) which could completely abolish the hypertensive effect of norepinephrine (1.0 micrograms) exerted a partial inhibition of the enhancement of PA release caused by dilazep; however, it did not affect those caused by other agents. Quinacrine (50 microM) and indomethacin (100 microM) did not have any effects on the enhancements of PA release caused by the five potentiators.

摘要

在离体灌注的猪耳中研究了血管活性药物对纤溶酶原激活剂(PA)释放的作用机制。在用含阿托品(3微摩尔)的台氏液灌注时,乙酰胆碱(1.0微克)引起的PA释放增强被完全抑制;然而,其他增强剂引起的增加,即缓激肽(1.0微克)、组胺(1.0微克)、地拉卓(30微克)和凝血酶(6单位)不受影响。在使用美吡拉敏(10微摩尔)的情况下,组胺(1.0微克)引起的PA释放增加被完全抑制;地拉卓(30微克)引起的增加被部分抑制,然而,乙酰胆碱、缓激肽和凝血酶引起的增加不受影响。能完全消除去甲肾上腺素(1.0微克)升压作用的罂粟碱(30微摩尔)对地拉卓引起的PA释放增强有部分抑制作用;然而,它对其他药物引起的增强作用没有影响。奎纳克林(50微摩尔)和吲哚美辛(100微摩尔)对这五种增强剂引起的PA释放增强没有任何作用。

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