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大鼠巨细胞网状核参与胍那苄引起的低血压、心肌收缩力降低及心动过缓。

Participation of nucleus reticularis gigantocellularis in guanabenz-promoted hypotension, decrease in cardiac contractility and bradycardia in rats.

作者信息

Lim H C, Chong O K, Chan S H

出版信息

Neuropharmacology. 1985 Dec;24(12):1241-6. doi: 10.1016/0028-3908(85)90160-1.

Abstract

The possible participation of the nucleus reticularis gigantocellularis in the hypotension, decrease in cardiac contractility and bradycardia induced by guanabenz was examined in rats that were anesthetized with pentobarbital sodium (40 mg/kg, i.p.). Guanabenz (10 micrograms/kg, i.v.) elicited an initial, transient hypertension, accompanied by an increase in cardiac contractility, followed by a significant and sustained hypotension, as well as decrease in the force and rate of cardiac contraction. In rats receiving bilateral focal electrolytic lesions of the nucleus reticularis gigantocellularis, the same injection produced only the initial transient responses, without the subsequent depressant effects. Microinjection of guanabenz directly into the ventro-medial portion of the nucleus reticularis gigantocellularis, at an ineffective systemic concentration (500 ng), produced significant and prolonged reduction in arterial pressure, cardiac contractility and heart rhythm. On the other hand, local application of the same concentration (500 ng) of guanabenz into the lateral portion of the same nucleus produced only minor hypotension and bradycardia, with no decrease in cardiac contractility. It is concluded that the nucleus reticularis gigantocellularis is at least one of the central sites through which guanabenz may produce its cardiovascular suppressant effects.

摘要

在以戊巴比妥钠(40毫克/千克,腹腔注射)麻醉的大鼠中,研究了巨细胞网状核在胍那苄诱导的低血压、心肌收缩力降低和心动过缓中可能的参与作用。胍那苄(10微克/千克,静脉注射)引起初始的、短暂的高血压,伴有心肌收缩力增加,随后是显著且持续的低血压,以及心肌收缩力和速率降低。在接受双侧巨细胞网状核局部电解损伤的大鼠中,相同注射仅产生初始的短暂反应,而无随后的抑制作用。以无效的全身浓度(500纳克)将胍那苄直接微量注射到巨细胞网状核的腹内侧部分,可使动脉压、心肌收缩力和心律显著且持续降低。另一方面,将相同浓度(500纳克)的胍那苄局部应用于同一核的外侧部分,仅产生轻微的低血压和心动过缓,心肌收缩力无降低。结论是,巨细胞网状核至少是胍那苄可能产生其心血管抑制作用的中枢部位之一。

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