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中杏仁核调节清醒大鼠的压力反射活动。

The medial amygdaloid nucleus modulates the baroreflex activity in conscious rats.

机构信息

Departments of Pharmacology, School of Medicine of Ribeirao Preto, University of São Paulo, Ribeirão Preto, SP 14090-090, Brazil.

Departments of Pharmacology, School of Medicine of Ribeirao Preto, University of São Paulo, Ribeirão Preto, SP 14090-090, Brazil.

出版信息

Auton Neurosci. 2015 Dec;193:44-50. doi: 10.1016/j.autneu.2015.07.003. Epub 2015 Jul 17.

Abstract

The medial amygdaloid nucleus (MeA) is involved in cardiovascular control. In the present study we report the effect of MeA pharmacological ablations caused by bilateral microinjections of the nonselective synaptic blocker CoCl2 on cardiac baroreflex responses in rats. MeA synaptic inhibition evoked by local bilateral microinjection of 100 nL of CoCl2 (1 mM) did not affect blood pressure or heart rate baseline, suggesting no tonic MeA influence on resting cardiovascular parameters. However, 10 min after CoCl2 microinjection into the MeA of male Wistar rats, the reflex bradycardic response evoked by intravenous infusion of phenylephrine was significantly enhanced when compared with the reflex bradycardic response observed before CoCl2. The treatment did not affect the tachycardic responses to the intravenous infusion of sodium nitroprusside (SNP). Baroreflex activity returned to control values 60 min after CoCl2 microinjections, confirming a reversible blockade. The present results indicate an involvement of the MeA in baroreflex modulation, suggesting that synapses in the MeA have an inhibitory influence on the bradycardic component of the baroreflex in conscious rats.

摘要

内侧杏仁核(MeA)参与心血管控制。在本研究中,我们报告了双侧微量注射非选择性突触阻滞剂 CoCl2 引起的 MeA 药理学消融对大鼠心脏压力反射反应的影响。MeA 突触抑制通过局部双侧微量注射 100nL CoCl2(1mM)诱发,不影响血压或心率基线,表明 MeA 对静息心血管参数没有紧张影响。然而,在雄性 Wistar 大鼠 MeA 内微量注射 CoCl2 10 分钟后,与 CoCl2 注射前观察到的反射性心动过缓反应相比,静脉注射苯肾上腺素引起的反射性心动过缓反应明显增强。该治疗方法不影响静脉注射硝普钠(SNP)引起的心动过速反应。CoCl2 微量注射 60 分钟后,反射活动恢复到对照值,证实了可逆性阻断。目前的结果表明 MeA 参与了压力反射调节,表明 MeA 中的突触对清醒大鼠压力反射的心动过缓成分具有抑制作用。

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