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离体灌流大鼠尾动脉的冷诱导血管舒张

Cold-induced vasodilatation in isolated, perfused rat tail artery.

作者信息

Gardner C A, Webb R C

出版信息

Am J Physiol. 1986 Jul;251(1 Pt 2):H176-81. doi: 10.1152/ajpheart.1986.251.1.H176.

DOI:10.1152/ajpheart.1986.251.1.H176
PMID:3728694
Abstract

This study characterizes an in vitro model of the "hunting response" (cold-induced vasoconstriction and vasodilatation). Two-centimeter segments of rat tail arteries (n = 15) were placed in a muscle bath (37 degrees C) and perfused (37 degrees C) at constant pressure (50 mmHg; flow = 14.5 +/- 0.8 ml/min) with physiological salt solution. Arteries constricted (23.7 +/- 2.8% decrease in flow) in response to activation of adrenergic nerves by electrical stimulation (9 V, 0.1-1.0 Hz, 0.1-4 ms). Cooling the bath to 4-12 degrees C (perfusate = 37 degrees C) caused further flow reduction (0-0.5 ml/min) in 14 arteries. After 20-40 min, 12 arteries dilated (7.4 +/- 1.2 ml/min) followed by constriction in 5-10 min. Typically, flow oscillated between periods of prolonged low flow and brief periods of high flow. Phentolamine (10(-6) M in bath) and acute adrenergic denervation blocked flow changes caused by decreased bath temperature. In unstimulated arteries, exogenous norepinephrine (6 X 10(-8) M in bath) decreased flow by 20%. On cooling (7-10 degrees C) flow decreased to zero, but did not oscillate. These results are consistent with the hypothesis that cold-induced vasoconstriction is caused by augmented smooth muscle responsiveness to norepinephrine, whereas cold-induced vasodilatation is caused by a cessation of transmitter release from adrenergic nerve endings.

摘要

本研究对“狩猎反应”(冷诱导的血管收缩和血管舒张)的体外模型进行了表征。将大鼠尾动脉的2厘米节段(n = 15)置于肌肉浴槽(37℃)中,并在恒定压力(50 mmHg;流量 = 14.5±0.8 ml/min)下用生理盐溶液在37℃进行灌注。通过电刺激(9 V,0.1 - 1.0 Hz,0.1 - 4 ms)激活肾上腺素能神经,动脉会发生收缩(流量减少23.7±2.8%)。将浴槽冷却至4 - 12℃(灌注液 = 37℃)会使14条动脉的流量进一步减少(0 - 0.5 ml/min)。20 - 40分钟后,12条动脉扩张(7.4±1.2 ml/min),随后在5 - 10分钟内收缩。通常,流量在长时间的低流量期和短时间的高流量期之间振荡。酚妥拉明(浴槽中浓度为10^(-6) M)和急性肾上腺素能去神经支配可阻断由浴槽温度降低引起的流量变化。在未受刺激的动脉中,外源性去甲肾上腺素(浴槽中浓度为6×10^(-8) M)可使流量降低20%。冷却至(7 - 10℃)时,流量降至零,但不会振荡。这些结果与以下假设一致,即冷诱导的血管收缩是由平滑肌对去甲肾上腺素的反应性增强引起的,而冷诱导的血管舒张是由肾上腺素能神经末梢递质释放停止引起的。

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