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电刺激大鼠舌咽神经诱发的心血管反射反应。

Reflex cardiovascular responses induced by electrical stimulation of glossopharyngeal nerves in the rat.

作者信息

Lee J Y, Walsh G M, Mokler C M, Tobia A J

出版信息

J Pharmacol Methods. 1981 Jan;5(1):15-27. doi: 10.1016/0160-5402(81)90098-x.

Abstract

Reflex cardiovascular responses to electrical stimulation of glossopharyngeal nerves (GPN) were studied in Dial-Urethane anesthetized rats. GPN stimulation at 3 V, 0.3 msec and 50 Hz produced maximal reflex depressor (34 +/- 2 mmHg) and bradycardia (21 +/- 2 beats/min) responses that were altered as follows: pentolinium (0.25 mg/kg, i.a.) blocked approximately 72% and 89% of control values of depressor and bradycardia responses, respectively; tripelennamine (5 mg/kg, i.a.) significantly reduced depressor responses (76%); whereas atropine (0.4 mg/kg i.a.) blocked only bradycardia (85%). Regional blood flow studies showed that GPN stimulation reduced systemic arterial pressure (approximately 25%), and increased iliac artery blood flow (5%), and decreased blood flow through the renal (14%) and superior mesenteric (13%) arteries. Hence, decreases in vascular resistance during GPN stimulation were greater in the hindlimb vascular bed (28%) than in the renal (14%) or the mesenteric vasculatures. In addition, the magnitude of decreases in hindlimb vascular resistance by GPN stimulation was reduced (80%) by pretreatment with tripelennamine, but not by atropine. The results suggest that reductions in arterial blood pressure and hindlimb vascular resistance of the rat in response to GPN stimulation may be mediated via a histaminergic vasodilator mechanism, and that there may be a differential pattern of reflex vascular adjustments of blood flow and vascular resistance among regional vasculatures of the rate.

摘要

在硫喷妥钠麻醉的大鼠中研究了舌咽神经(GPN)电刺激引起的反射性心血管反应。以3V、0.3毫秒和50赫兹刺激GPN可产生最大反射性降压(34±2 mmHg)和心动过缓(21±2次/分钟)反应,这些反应的变化如下:潘托铵(0.25mg/kg,腹腔注射)分别阻断了约72%和89%的对照值的降压和心动过缓反应;曲吡那敏(5mg/kg,腹腔注射)显著降低了降压反应(76%);而阿托品(0.4mg/kg腹腔注射)仅阻断了心动过缓(85%)。局部血流研究表明,GPN刺激降低了全身动脉压(约25%),增加了髂动脉血流量(5%),并减少了通过肾动脉(14%)和肠系膜上动脉(13%)的血流量。因此,GPN刺激期间后肢血管床(28%)的血管阻力下降幅度大于肾血管(14%)或肠系膜血管。此外,用曲吡那敏预处理可降低GPN刺激引起的后肢血管阻力下降幅度(80%),但阿托品则不能。结果表明,大鼠对GPN刺激的动脉血压和后肢血管阻力降低可能通过组胺能血管舒张机制介导,并且大鼠各区域血管之间的血流和血管阻力反射性血管调节模式可能存在差异。

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