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胍乙啶诱导的肾上腺素能交感神经切除术可增加神经内膜灌注并降低神经内膜微血管阻力。

Guanethidine-induced adrenergic sympathectomy augments endoneurial perfusion and lowers endoneurial microvascular resistance.

作者信息

Zochodne D W, Huang Z X, Ward K K, Low P A

机构信息

Neurobiology Laboratory, Mayo Clinic, Rochester, MN 55905.

出版信息

Brain Res. 1990 Jun 11;519(1-2):112-7. doi: 10.1016/0006-8993(90)90067-l.

Abstract

Chronic administration of guanethidine sulfate in the rat induces a selective adrenergic neuropathy. We studied the effects of guanethidine-induced adrenergic sympathectomy on rat sciatic nerve blood flow (NBF), microvascular resistance (MR), vessel caliber and norepinephrine (NE) content. A control group of animals was studied following chronic administration of mammalian Ringer's solution. NBF and MR were measured with an endoneurial microelectrode, using the technique of hydrogen clearance (HC). Following HC, the sciatic nerve was perfused with India Ink, removed, frozen and sectioned. Measurements were made of endoneurial microvessel numbers, diameter, circumference and area. The contralateral sciatic nerve was removed for measurements of NE content. In guanethidine-treated animals we observed elevated NBF, reduced MR and dilated microvessels. Numbers of microvessels and fascicular areas were similar to controls. NE content was markedly reduced following sympathectomy. These studies suggest that NBF, unlike cerebral blood flow (CBF), is regulated by its adrenergic input. Removal of adrenergic innervation of the vasa nervorum appears to result in a loss of tonic vasoconstrictive action.

摘要

在大鼠中长期给予硫酸胍乙啶会诱发一种选择性肾上腺素能神经病变。我们研究了胍乙啶诱导的肾上腺素能交感神经切除术对大鼠坐骨神经血流量(NBF)、微血管阻力(MR)、血管口径和去甲肾上腺素(NE)含量的影响。对一组经长期给予哺乳动物林格氏液的动物进行了研究。使用氢清除(HC)技术,通过神经内膜微电极测量NBF和MR。HC后,用印度墨水灌注坐骨神经,取出、冷冻并切片。测量神经内膜微血管数量、直径、周长和面积。取出对侧坐骨神经用于测量NE含量。在胍乙啶处理的动物中,我们观察到NBF升高、MR降低和微血管扩张。微血管数量和束状区域与对照组相似。交感神经切除术后NE含量明显降低。这些研究表明,与脑血流量(CBF)不同,NBF受其肾上腺素能输入的调节。去除神经血管的肾上腺素能神经支配似乎会导致紧张性血管收缩作用丧失。

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