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松节油反向刺激作用机制的进一步研究。

Further studies of the mechanism of counter irritation by turpentine.

作者信息

Damas J, Remacle-Volon G, Deflandre E

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1986 Feb;332(2):196-200. doi: 10.1007/BF00511412.

Abstract

The influence of counter irritation by turpentine (0.2 ml) on zymosan- and carrageenan-oedemas was investigated in the rat. Zymosan-oedema was inhibited by mepyramine and methysergide and by leucopenia. It was not modified by captopril and developed normally in kininogendeficient Brown Norway rats. Leucocytes and mast cell amines but not kinins are thus involved in zymosan-oedema. The last phase of this reaction was inhibited by counter irritation alone, but the odema was largely depressed by counter irritation in rats pretreated with mepyramine and methysergide. Carrageenan-oedema was increased by kininase inhibitors and inhibited by leucopenia in normal rats. This inflammatory reaction had a small developement and was not increased by kininase inhibitors in kininogen-deficient BN rats. Leucocytes and kinins participate in the developement of this inflammatory reaction in normal rats while kinins are lacking in deficient rats. Counter irritation depressed carrageenan-oedema in deficient Brown Norway rats and suppressed the potentiating effect of kininase inhibitors in normal rats. Carrageenan oedema was nearly abolished in turpentine-treated leucopenic rats. These results suggest that the anti-inflammatory effect of counter irritation by turpentine could depend on a reduction of leucocyte accumulation into zymosan-oedema and on a reduction of both kinin formation and of leucocyte accumulation into carrageenan-oedema. The significance of T-kininogen as acute phase reactant is discussed.

摘要

在大鼠中研究了松节油(0.2毫升)反向刺激对酵母聚糖和角叉菜胶性水肿的影响。组胺和甲基麦角新碱以及白细胞减少可抑制酵母聚糖性水肿。卡托普利对其无影响,且在激肽原缺乏的棕色挪威大鼠中其正常发展。因此,白细胞和肥大细胞胺而非激肽参与了酵母聚糖性水肿。该反应的最后阶段仅通过反向刺激被抑制,但在用组胺和甲基麦角新碱预处理的大鼠中,反向刺激可使水肿大幅减轻。在正常大鼠中,激肽酶抑制剂可增加角叉菜胶性水肿,白细胞减少可抑制之。在激肽原缺乏的BN大鼠中,这种炎症反应发展较小,且激肽酶抑制剂不会使其增加。在正常大鼠中,白细胞和激肽参与了这种炎症反应的发展,而在缺乏激肽原的大鼠中则缺乏激肽。反向刺激可减轻缺乏激肽原的棕色挪威大鼠的角叉菜胶性水肿,并抑制正常大鼠中激肽酶抑制剂的增强作用。在经松节油处理的白细胞减少的大鼠中,角叉菜胶性水肿几乎消失。这些结果表明,松节油反向刺激的抗炎作用可能取决于减少白细胞向酵母聚糖性水肿中的积聚,以及减少激肽形成和白细胞向角叉菜胶性水肿中的积聚。讨论了T-激肽原作为急性期反应物的意义。

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