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豚鼠大脑小动脉的血管舒张神经支配

Vasodilator innervation of small cerebral arteries of guinea pigs.

作者信息

Saito A, Goto K

机构信息

Department of Pharmacology, University of Tsukuba, Ibaraki, Japan.

出版信息

J Auton Nerv Syst. 1994 Sep;49 Suppl:S59-62. doi: 10.1016/0165-1838(94)90088-4.

Abstract

The neuronal influence on the resistance of cerebral arteries was analyzed in middle cerebral arteries of guinea pigs. Calcitonin gene-related peptide- and vasoactive intestinal peptide-immunoreactive nerves and NADPH-diaphorase-positive nerves were present in the distal portion of the middle cerebral artery. Isolated middle cerebral arteries were cannulated and perfused at a constant flow rate (1 ml/min) and the perfusion pressure was monitored. Prostaglandin F2 alpha (PGF2 alpha) and K+ (50 mM) elicited a sustained increase of the perfusion pressure (vasoconstriction), while noradrenaline and 5-hydroxytryptamine caused only a slight constriction. Electrical field stimulation (FS) at 8 Hz did not elicit a contractile response. In tissues precontracted with PGF2 alpha, FS induced a tetrodotoxin-sensitive vasodilator response. Endothelium-denudation and removal of the effect of sensory nerves by capsaicin-treatment did not affect the FS-induced vasodilation. In contrast, nitro-L-arginine, an inhibitor of NO formation, attenuated the FS-induced vasodilatation. These results show that the resistance of the cerebral vessels of guinea pigs is under the influence of vasodilator nerves and that the neurogenic vasodilator mechanism involves NO synthesis.

摘要

在豚鼠大脑中动脉中分析了神经元对脑动脉阻力的影响。降钙素基因相关肽和血管活性肠肽免疫反应性神经以及NADPH - 黄递酶阳性神经存在于大脑中动脉的远端部分。分离的大脑中动脉插管后以恒定流速(1 ml/min)灌注,并监测灌注压力。前列腺素F2α(PGF2α)和K⁺(50 mM)引起灌注压力持续升高(血管收缩),而去甲肾上腺素和5 - 羟色胺仅引起轻微收缩。8 Hz的电场刺激(FS)未引起收缩反应。在预先用PGF2α收缩的组织中,FS诱导了对河豚毒素敏感的血管舒张反应。内皮剥脱和用辣椒素处理消除感觉神经的作用并不影响FS诱导的血管舒张。相反,一氧化氮形成抑制剂硝基 - L - 精氨酸减弱了FS诱导的血管舒张。这些结果表明,豚鼠脑血管阻力受血管舒张神经的影响,并且神经源性血管舒张机制涉及一氧化氮合成。

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