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猫坐骨神经刺激诱发逆行性血管舒张的介质研究。

A study on the mediators of antidromic vasodilatation elicited by sciatic nerve stimulation in cats.

作者信息

Küçükhüseyin C, Kayaalp S O

机构信息

University of Istanbul, Faculty of Medicine, Department of Pharmacology, Istanbul/Ankara, Turkey.

出版信息

J Basic Clin Physiol Pharmacol. 1996;7(4):363-73. doi: 10.1515/jbcpp.1996.7.4.363.

Abstract

This study was undertaken to ascertain whether a purinergic substance, histamine, dopamine or prostaglandins are mediators involved in antidromic vasodilatation. This type of vasodilatation was elicited by stimulation of the distal end of sectioned sciatic nerve at 40 V with 2 msec pulses for 30 sec in autoperfused hindlimb of reserpine-pretreated and anesthetized cats. Artificial respiration was applied because of curarization that was done to abolish the vascular responses due to contractions of striated muscle. Stimulation of sciatic nerve caused a sustained vasodilatation which was more marked at a frequency of 30 pps. The responsiveness of the perfused vessels to vasodilator stimuli tended to increase by increasing the duration of perfusion as controlled by papaverine administration at certain intervals. Both mepyramine and subsequent administration of metiamide did not produce any change in the vasodilator response to nerve stimulation though they blocked the vasodilator response to histamine. Dopamine injected intra-arterially elicited a pressor response which was reversed into a vasodilator one by phentolamine. This vasodilator response to dopamine tended to be reduced by haloperidol which produced either no change or a slight increase in antidromic vasodilatation. Pretreatment with theophylline to antagonize the likely purinergic mediators or with indomethacin to inhibit the synthesis of prostaglandins had no effect on antidromic vasodilatation elicited by sciatic nerve stimulation. These results suggest that the above-mentioned compounds might not be involved in antidromic vasodilatation.

摘要

本研究旨在确定嘌呤能物质、组胺、多巴胺或前列腺素是否为参与逆向血管舒张的介质。在利血平预处理并麻醉的猫的自灌注后肢中,以40伏、2毫秒脉冲刺激切断的坐骨神经远端30秒,引发这种类型的血管舒张。由于使用箭毒进行了肌松处理以消除横纹肌收缩引起的血管反应,因此采用了人工呼吸。刺激坐骨神经会引起持续的血管舒张,在30次/秒的频率下更为明显。通过间隔给予罂粟碱控制灌注持续时间,灌注血管对血管舒张刺激的反应性倾向于增加。尽管美吡拉敏和随后给予的甲硫咪胺阻断了对组胺的血管舒张反应,但它们对神经刺激引起的血管舒张反应没有产生任何变化。动脉内注射多巴胺会引发升压反应,酚妥拉明可将其逆转成血管舒张反应。氟哌啶醇使这种对多巴胺的血管舒张反应倾向于降低,而对逆向血管舒张没有变化或略有增加。用茶碱拮抗可能的嘌呤能介质或用吲哚美辛抑制前列腺素合成的预处理,对坐骨神经刺激引起的逆向血管舒张没有影响。这些结果表明上述化合物可能不参与逆向血管舒张。

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