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犬心脏中窦房结心率及房室传导的不同交感 - 副交感神经相互作用

Different sympathetic-parasympathetic interactions on sinus rate and atrioventricular conduction in dog hearts.

作者信息

Furukawa Y, Takei M, Narita M, Karasawa Y, Tada A, Zenda H, Chiba S

机构信息

Department of Pharmacology, Shinshu University School of Medicine, Matsumoto, Japan.

出版信息

Eur J Pharmacol. 1997 Sep 10;334(2-3):191-200. doi: 10.1016/s0014-2999(97)01177-1.

Abstract

We investigated the sympathetic-parasympathetic interactions involved in SA nodal pacemaker activity and AV conductivity in the anesthetized dog heart. Stimulation of the intracardiac parasympathetic nerves to the SA nodal region (SAPS) and stimulation of the intracardiac parasympathetic nerves to the AV nodal region (AVPS) induced negative chronotropic and dromotropic responses, respectively. Cardiac sympathetic stimulation, aminophylline, 3-isobutyl-1-methylxanthine (IBMX, a relatively pure nonselective phosphodiesterase inhibitor) and methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-p iridine-5-carboxylate (Bay k 8644, a Ca2+ channel agonist) increased sinus rate and decreased AV conduction time. Sympathetic stimulation augmented the negative chronotropic response to SAPS but not the negative dromotropic response to AVPS, IBMX augmented both responses, Bay k 8644 augmented the chronotropic response and attenuated the dromotropic response, and aminophylline did not affect the chronotropic response to SAPS and inhibited the dromotropic response to AVPS. Additionally, when Bay k 8644 directly given via the AV node artery decreased AV conduction time, it attenuated the negative dromotropic response to AVPS and carbachol injected into the AV node artery. These results suggest that the differential sympathetic-parasympathetic interactions on sinus rate and AV conduction are at least partly induced by an interaction between changes in slow inward Ca2+ current or intracellular Ca2+ and the cardiac effects of acetylcholine in the heart in situ.

摘要

我们研究了麻醉犬心脏中窦房结起搏活动和房室传导所涉及的交感 - 副交感相互作用。刺激心脏内通向窦房结区域的副交感神经(SAPS)和刺激心脏内通向房室结区域的副交感神经(AVPS)分别引起负性变时性和负性变传导性反应。心脏交感神经刺激、氨茶碱、3 - 异丁基 - 1 - 甲基黄嘌呤(IBMX,一种相对纯的非选择性磷酸二酯酶抑制剂)和甲基 - 1,4 - 二氢 - 2,6 - 二甲基 - 3 - 硝基 - 4 -(2 - 三氟甲基苯基)- 吡啶 - 5 - 羧酸酯(Bay k 8644,一种Ca2 +通道激动剂)增加窦性心率并缩短房室传导时间。交感神经刺激增强了对SAPS的负性变时性反应,但未增强对AVPS的负性变传导性反应;IBMX增强了两种反应;Bay k 8644增强了变时性反应并减弱了变传导性反应;氨茶碱不影响对SAPS的变时性反应,并抑制对AVPS的变传导性反应。此外,当通过房室结动脉直接给予Bay k 8644缩短房室传导时间时,它减弱了对AVPS和注入房室结动脉的卡巴胆碱的负性变传导性反应。这些结果表明,交感 - 副交感对窦性心率和房室传导的差异性相互作用至少部分是由原位心脏中慢内向Ca2 +电流或细胞内Ca2 +变化与乙酰胆碱的心脏效应之间的相互作用所诱导的。

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