Sympathetic afferent stimulation inhibits central vagal activation induced by intravenous medetomidine in rats
Sympathetic afferent stimulation inhibits central vagal activation induced by intravenous medetomidine in rats
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DOI：
10.1111/apha.12123
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发表时间：
2013-09-01
影响因子：
6.3
通讯作者：
Sugimachi, M.
中科院分区：
文献类型：
--
作者：
Kawada, T.;Akiyama, T.;Sugimachi, M.
目的：检查交感传入刺激（SAS）是否抑制α（2）-肾上腺素能刺激引起的中枢迷走神经激活。方法：在麻醉的Wistar-Kyoto大鼠中，对左心室应用心脏微透析技术，并在无交感神经传入刺激（SAS）的情况下检查美托咪定的α（2）-肾上腺素刺激对心肌间质乙酰胆碱（ACh）水平的影响（n = 6) 或存在 (n = 6) 从左侧星状神经节传递的 SAS。在不存在或存在 SAS 的情况下，还检查了迷走神经传出电刺激对心肌间质 ACh 释放的影响 (n = 6)。结果：在不存在 SAS 的情况下，静脉注射美托咪定 (0.1 mg kg(-1)) 显着增加了心肌间质 ACh 水平（从 1.95 +/- 0.79 到 3.36 +/- 1.61 nM，P < 0.05），但不存在 SAS（从 1.67 +/- 0.67 到 2.01 +/- 0.78 nM）。相比之下，无论是否有 SAS，迷走神经电刺激都能将心肌间质 ACh 水平提高到相同程度（无 SAS 时为 1.66 +/- 0.16 至 3.93 +/- 0.72 nM，有 SAS 时为 4.05 +/- 0.89 nM）。结论：交感传入刺激抑制美托咪定诱导的 ACh 释放，但不抑制电刺激诱导的 ACh 释放，表明 SAS通过中枢机制抑制美托咪定诱导的迷走神经激活。虽然α(2)-肾上腺素能激动剂激活中枢迷走神经可以替代迷走神经电激活，但阻断交感神经传入输入对于提高α(2)-肾上腺素能激动剂增强迷走神经活动的功效可能很重要。
Aim: To examine whether sympathetic afferent stimulation (SAS) inhibits central vagal activation induced by alpha(2)-adrenergic stimulation.Methods: In anaesthetized Wistar-Kyoto rats, a cardiac microdialysis technique was applied to the left ventricle, and the effect of alpha(2)-adrenergic stimulation by medetomidine on myocardial interstitial acetylcholine (ACh) levels was examined in the absence (n = 6) or the presence (n = 6) of SAS delivered from the left stellate ganglion. The effect of electrical vagal efferent stimulation on myocardial interstitial ACh release was also examined in the absence or the presence of SAS (n = 6).Results: Intravenous medetomidine (0.1 mg kg(-1)) significantly increased myocardial interstitial ACh levels in the absence of SAS (from 1.95 +/- 0.79 to 3.36 +/- 1.61 nM, P < 0.05), but not in the presence of SAS (from 1.67 +/- 0.67 to 2.01 +/- 0.78 nM). In contrast, electrical vagal nerve stimulation increased myocardial interstitial ACh level to the same degree regardless of SAS (from 1.66 +/- 0.16 to 3.93 +/- 0.72 nM without SAS vs. 4.05 +/- 0.89 nM with SAS).Conclusion: Sympathetic afferent stimulation inhibited medetomidine-induced ACh release, but not electrical stimulation-induced ACh release, suggesting that SAS inhibited medetomidine-induced vagal activation via central mechanisms. While central vagal activation by alpha(2)-adrenergic agonists could be an alternative to electrical vagal activation, blocking sympathetic afferent input may be important to increase the efficacy of alpha(2)-adrenergic agonists in enhancing vagal nerve activity.