Suppr超能文献

通过抑制延髓尾端腹外侧部产生的动脉血压下降:尾端加压区。

A fall in arterial blood pressure produced by inhibition of the caudalmost ventrolateral medulla: the caudal pressor area.

作者信息

Possas O S, Campos R R, Cravo S L, Lopes O U, Guertzenstein P G

机构信息

Department of Physiology, Escola Paulista de Medicina, São Paulo, Brazil.

出版信息

J Auton Nerv Syst. 1994 Nov;49(3):235-45. doi: 10.1016/0165-1838(94)90170-8.

Abstract

The caudal edge of the ventrolateral medulla was mapped to localize sites where microinjections of L-glutamate (L-glu) produce pressor responses in paralyzed and artificially ventilated urethane-anesthetized rats. Pressor responses ranging from 15 to 65 mmHg were obtained when L-Glu (0.25 M, 200 nl) was microinjected in the ventral medullary surface within an area localized between the rootlets of the XII and first cervical nerves, lateral to the pyramids and just medial to the spinal roots of the XI cranial nerve. This area has been called the caudal pressor area (CPA). Inhibition of the CPA by microinjection of GABA or glycine resulted in marked falls (15-45 mmHg) of arterial blood pressure (AP). Hypotension in response to CPA inhibition was also obtained in unanesthetized decerebrate animals. Cardiovascular responses to CPA stimulation or inhibition depend on the activity of neurons in the rostral ventrolateral medulla (RVLM). During hypotension provoked by RVLM inhibition, pressor responses to CPA stimulation were abolished. Conversely, pressor responses to RVLM stimulation were maintained during hypotension produced by inhibition of CPA. Pressor response to bilateral carotid occlusion were not reduced by CPA inhibition. We conclude that cells in the caudal most ventrolateral medulla exert a tonic pressor activity that contributes to maintenance of basal levels of the vasomotor tone and arterial blood pressure, its inhibition, however, does not prevent the pressor response to carotid occlusion.

摘要

绘制延髓腹外侧尾端区域图,以定位在瘫痪并人工通气的氨基甲酸乙酯麻醉大鼠中微量注射L - 谷氨酸(L - glu)产生升压反应的部位。当在第十二对脑神经和第一颈神经小根之间、锥体外侧且恰在第十一脑神经脊髓根内侧的腹侧延髓表面区域微量注射L - Glu(0.25 M,200 nl)时,可获得15至65 mmHg的升压反应。该区域被称为尾侧升压区(CPA)。微量注射GABA或甘氨酸抑制CPA会导致动脉血压(AP)显著下降(15 - 45 mmHg)。在未麻醉的去大脑动物中也可观察到因CPA抑制引起的低血压。对CPA刺激或抑制的心血管反应取决于延髓头端腹外侧(RVLM)神经元的活动。在RVLM抑制引起的低血压期间,对CPA刺激的升压反应消失。相反,在CPA抑制产生的低血压期间,对RVLM刺激的升压反应得以维持。CPA抑制不会降低对双侧颈动脉闭塞的升压反应。我们得出结论,延髓最尾端腹外侧的细胞发挥着紧张性升压活动,这有助于维持血管运动张力和动脉血压的基础水平,然而,对其抑制并不妨碍对颈动脉闭塞的升压反应。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验