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尾侧加压区和延髓头端腹外侧区内兴奋性氨基酸受体的阻断会改变大鼠对中缝隐核刺激的心血管反应。

Excitatory amino acid receptor blockade within the caudal pressor area and rostral ventrolateral medulla alters cardiovascular responses to nucleus raphe obscurus stimulation in rats.

作者信息

Silva N F, Pires J G P, Dantas M A, Futuro Neto H A

机构信息

Associaço Educacional de Vitória (FAESA), Vitória, ES, Brasil.

出版信息

Braz J Med Biol Res. 2002 Oct;35(10):1237-45. doi: 10.1590/s0100-879x2002001000019. Epub 2002 Oct 13.

Abstract

Pressor responses elicited by stimulation of the nucleus raphe obscurus (NRO) depend on the integrity of the rostral ventrolateral medulla (RVLM). Therefore, to test the participation of excitatory amino acid (EAA) receptors in the cardiovascular responses evoked by NRO stimulation (1 ms, 100 Hz, 40-70 microA, for 10 s), the EAA antagonist kynurenic acid (Kyn) was microinjected at different sites in the ventrolateral medullar surface (2.7 nmol/200 nl) of male Wistar rats (270-320 g, N = 39) and NRO stimulation was repeated. The effects of NRO stimulation were: hypertension (deltaMAP = +43 +/- 1 mmHg, P<0.01), bradycardia (deltaHR = -30 +/- 7 bpm, P<0.01) and apnea. Bilateral microinjection of Kyn into the RVLM, which did not change baseline parameters, almost abolished the bradycardia induced by NRO stimulation (deltaHR = -61 +/- 3 before vs -2 +/- 3 bpm after Kyn, P<0.01, N = 7). Unilateral microinjection of Kyn into the CVLM did not change baseline parameters or reduce the pressor response to NRO stimulation (deltaMAP = +46 +/- 5 before vs +48 +/- 5 mmHg after Kyn, N = 6). Kyn bilaterally microinjected into the caudal pressor area reduced blood pressure and heart rate and almost abolished the pressor response to NRO stimulation (deltaMAP = +46 +/- 4 mmHg before vs +4 +/- 2 mmHg after Kyn, P<0.01, N = 7). These results indicate that EAA receptors on the medullary ventrolateral surface play a role in the modulation of the cardiovascular responses induced by NRO stimulation, and also suggest that the RVLM participates in the modulation of heart rate responses and that the caudal pressor area modulates the pressor response following NRO stimulation.

摘要

刺激中缝隐核(NRO)所引发的升压反应取决于延髓头端腹外侧区(RVLM)的完整性。因此,为了测试兴奋性氨基酸(EAA)受体在NRO刺激(1毫秒,100赫兹,40 - 70微安,持续10秒)所诱发的心血管反应中的作用,将EAA拮抗剂犬尿氨酸(Kyn)微量注射到雄性Wistar大鼠(270 - 320克,N = 39)延髓腹外侧表面的不同部位(2.7纳摩尔/200纳升),并重复进行NRO刺激。NRO刺激的效应包括:高血压(平均动脉压变化量 = +43 ± 1毫米汞柱,P<0.01)、心动过缓(心率变化量 = -30 ± 7次/分钟,P<0.01)以及呼吸暂停。向RVLM双侧微量注射Kyn,这并未改变基线参数,几乎完全消除了NRO刺激所诱发的心动过缓(注射Kyn前心率变化量 = -61 ± 3次/分钟,注射后为 -2 ± 3次/分钟,P<0.01,N = 7)。向尾端腹外侧延髓(CVLM)单侧微量注射Kyn既未改变基线参数,也未降低对NRO刺激的升压反应(注射Kyn前平均动脉压变化量 = +46 ± 5毫米汞柱,注射后为 +48 ± 5毫米汞柱,N = 6)。向尾侧升压区双侧微量注射Kyn可降低血压和心率,并且几乎完全消除了对NRO刺激的升压反应(注射Kyn前平均动脉压变化量 = +46 ± 4毫米汞柱,注射后为 +4 ± 2毫米汞柱,P<0.01,N = 7)。这些结果表明,延髓腹外侧表面的EAA受体在调节NRO刺激所诱发的心血管反应中发挥作用,同时也表明RVLM参与心率反应的调节,并且尾侧升压区在NRO刺激后调节升压反应。

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