Effects of sympathetic histamine on vasomotor responses of blood vessels in rabbit ear to electrical stimulation
Effects of sympathetic histamine on vasomotor responses of blood vessels in rabbit ear to electrical stimulation
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DOI：
10.1007/s12264-010-1126-6
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发表时间：
2010
影响因子：
5.6
通讯作者：
Ying-Ying Chen 陈瑛瑛-Ying;Jun Lv 吕军;Xiao-Yan Xue 薛小燕;Gong-Hao He 何功浩;Ying Zhou 周颖;Min Jia 贾敏;Xiao-Xing Luo 罗晓星
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文献类型：
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作者：
Ying-Ying Chen 陈瑛瑛-Ying;Jun Lv 吕军;Xiao-Yan Xue 薛小燕;Gong-Hao He 何功浩;Ying Zhou 周颖;Min Jia 贾敏;Xiao-Xing Luo 罗晓星
目的观察组胺受体拮抗剂对电刺激耳后神经引起的血管收缩反应的影响，探讨交感组胺对兔耳血管平滑肌收缩反应的突触前和突触后作用。方法将电刺激仪分别以10 Hz、20 Hz和40 Hz作用于兔耳后神经。在恒定灌流压下，用不同的组胺受体拮抗剂灌流全耳，观察灌流液流速的变化。结果3种频率的电刺激均能降低静脉流出道流速。H1受体拮抗剂扑尔敏可部分抑制ES引起的20 Hz和40 Hz的血管收缩（P < 0.05）。用肥大细胞特异性脱乙酰化合物48/80预处理肥大细胞，使肥大细胞内组胺耗竭后，扑尔敏仍能抑制ES引起的流速降低。而H2受体拮抗剂西咪替丁则可增强40 Hz ES引起的流速下降（P < 0.05）。H3受体拮抗剂硫代哌丁胺可增强ES在3个频率引起的血管收缩反应（P < 0.05）。结论刺激耳神经可引起交感神经释放组胺，而不是肥大细胞。此外，交感组胺的功能通过激活不同的组胺受体从突触前调节到突触后血管收缩或血管舒张而变化。
Objective To investigate the effects of histamine receptor antagonists on vasoconstriction induced by electrical stimulation (ES) on posterior auricular nerve, and to explore the pre- and post-synaptic effects of sympathetic histamine on the vasomotor responses of vascular smooth muscle in rabbit ear. Methods ES was applied to posterior auricular nerves of the whole rabbit ear at 10 Hz, 20 Hz and 40 Hz, respectively. Besides, the whole ear was perfused with different histamine receptor antagonists under constant perfusion pressure, and the changes in the flow rate of perfusate were observed. Results The flow rate of venous outflow was decreased by ES at all the 3 frequencies. The ES-induced vasoconstriction at 20 Hz and 40 Hz could be partly inhibited by H1 receptor antagonist chlorpheniramine (P < 0.05). After exhaustion of histamine in mast cells by pretreatment with specific mast cell degranulator compound 48/80, chlorpheniramine could still inhibit the ES-induced flow rate reduction. In contrast, H2 receptor antagonist cimetidine could enhance the 40-Hz ES-induced flow rate reduction (P < 0.05). Moreover, ES-induced vasoconstriction at the 3 frequencies could all be enhanced by H3 receptor antagonist thioperamide (P < 0.05). Conclusion Stimulation on the auricular nerve may evoke histamine release from sympathetic nerves rather than from mast cells. Moreover, the functions of sympathetic histamine vary from pre-synaptic modulation to post-synaptic vasoconstriction or vasodilatation, via activation of different histamine receptors.