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声音刺激诱发兔耳中央动脉的血管运动反射。

Sound stimulation-induced vasomotor reflex in the central artery of the rabbit ear.

作者信息

Takeoka M, Ueda G, Taguchi K, Ge R L, Terasawa K, Tsuchiya K

机构信息

Department of Oto-laryngology, Shinshu University School of Medicine, Matsumoto, Japan.

出版信息

Tohoku J Exp Med. 1996 Feb;178(2):101-11. doi: 10.1620/tjem.178.101.

Abstract

Effects of sound stimulation on the central artery of the rabbit ear were studied as a somato-autonomic reflex. Vasoconstriction and dilatation, caused by metronome sound stimulation, were estimated from the temperature fluctuations in the central artery of the ear, measured by a thermistor. To enhance the detection of temperature rises, moderately high background levels of arterial tone were established by exposing the tips of the ears to water at a temperature of 10 degrees C or 5 degrees C, prior to sound stimulation. A fall in arterial temperature due to vasoconstriction was observed immediately after the start of the 1-min sound stimulation, with a subsequent temperature rise which overshot the original basal level due to vasodilatation. A positive correlation between the ear temperature before sound stimulation and the temperature fall (p < 0.01), and a negative correlation between the ear temperature and the temperature rise (p < 0.05) were obtained. The temperature fall was blocked by phenoxybenzamine (9 mg/kg, i.p., p < 0.01). The subsequent rise was not influenced by atropine (3 mg/kg, i.p.) or phenoxybenzamine, however, it was attenuated by hexamethonium (6 mg/kg, i.p., p < 0.05). The temperature fall at the beginning of sound stimulation was related to alpha-adrenergic mechanism. The subsequent temperature rise was thought to be related to parasympathetic mechanism, excluding cholinergic mechanism.

摘要

作为一种躯体自主反射,研究了声音刺激对兔耳中央动脉的影响。通过由热敏电阻测量的耳中央动脉温度波动来估计由节拍器声音刺激引起的血管收缩和扩张。为了增强对温度升高的检测,在声音刺激之前,通过将兔耳尖端暴露于10摄氏度或5摄氏度的水中来建立适度较高的动脉张力背景水平。在1分钟声音刺激开始后立即观察到由于血管收缩导致的动脉温度下降,随后由于血管扩张温度上升超过了原始基础水平。声音刺激前的耳温与温度下降之间呈正相关(p < 0.01),耳温与温度上升之间呈负相关(p < 0.05)。温度下降被酚苄明(9毫克/千克,腹腔注射,p < 0.01)阻断。然而,随后的温度上升不受阿托品(3毫克/千克,腹腔注射)或酚苄明的影响,但被六甲铵(6毫克/千克,腹腔注射,p < 0.05)减弱。声音刺激开始时的温度下降与α-肾上腺素能机制有关。随后的温度上升被认为与副交感神经机制有关,不包括胆碱能机制。

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