Neurogenic vasodilator control of rabbit ear blood flow.

Neurogenic vasodilator control of rabbit ear blood flow.
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兔耳血流的神经源性血管扩张剂控制。

DOI:
10.1152/ajpregu.1992.262.5.r766
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发表时间:
1992
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Bishop,VS
Bishop,VS
中科院分区:
--
文献类型:
--
作者:
Taylor,WF;DiCarlo,SE;Bishop,VS

文献摘要

被引文献

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兔耳血流起体温调节作用。本研究的目的是确定兔耳血流量的增加,是由于体内温度(Ti)升高约2摄氏度(38.0-40.0摄氏度),是由于血管舒张活性还是肾上腺素能血管收缩活性的消退。将脉冲多普勒血流探头长期置于新西兰大白兔左右耳中央动脉,测量耳血流速度(EBF, kHz)。导管也被放置在一只枕动脉,选择性地给一只耳朵注射α 1-肾上腺素能拮抗剂,而对侧耳朵作为对照。在高温(H)(直肠温度升高)期间,α 1-肾上腺素能阻断对最大EBF没有影响(前5.95 +/- 0.87 kHz vs后6.11 +/- 1.04 kHz)。然而,α 1-肾上腺素能阻断使正常体温下静息EBF从0.18 +/- 0.04 kHz增加到1.23 +/- 0.27 kHz (P < 0.05),表明α 1-肾上腺素能张力的降低可能占加热期间EBF增加的约20%。第二个方案旨在确定耳神经阻断是否会改变EBF对H的反应。在H期间EBF最大时,向耳神经周围组织注射生理盐水或普鲁卡因胺。注射普鲁卡因胺使对侧耳EBF由5.99 +/- 0.87降低至0.48 +/- 0.19 kHz,而注射生理盐水对对侧耳EBF无影响(注射前4.33 +/- 1.16 kHz,注射后3.97 +/- 1.04 kHz)。(摘要删节250字)
Ear blood flow subserves thermoregulation in the rabbit. The purpose of this study was to determine if the increase in rabbit ear blood flow, in response to increases in internal temperature (Ti) of approximately 2 degrees C (38.0-40.0 degrees C), is due to an active vasodilation or a withdrawal of adrenergic vasoconstrictor activity. New Zealand White rabbits were chronically instrumented with a pulse Doppler flow probe on the central ear artery of the left and right ear for the measurement of ear blood flow velocity (EBF, kHz). Catheters were also positioned in one occipital artery for selective administration of an alpha 1-adrenergic antagonist to one ear, while the contralateral ear served as a control. During hyperthermia (H) (increase in rectal temperature) alpha 1-adrenergic blockade had no effect on the maximum EBF (5.95 +/- 0.87 before vs. 6.11 +/- 1.04 kHz after). However, alpha 1-adrenergic blockade increased resting EBF during normothermia from 0.18 +/- 0.04 to 1.23 +/- 0.27 kHz (P less than 0.05), suggesting that a decrease in alpha 1-adrenergic tone may account for approximately 20% of the increase in EBF during heating. The second protocol was designed to determine if blockade of the auricular nerve would alter EBF response to H. During maximum EBF during H, saline or procainamide was injected in the tissue surrounding the auricular nerve. Injection of procainamide decreased EBF from 5.99 +/- 0.87 to 0.48 +/- 0.19 kHz, while injection of saline had no effect on EBF of the contralateral ear (4.33 +/- 1.16 before vs. 3.97 +/- 1.04 kHz after).(ABSTRACT TRUNCATED AT 250 WORDS)