Cardiovascular effects produced by L-glutamate stimulation of the lateral hypothalamic area.
Cardiovascular effects produced by L-glutamate stimulation of the lateral hypothalamic area.
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L-谷氨酸刺激下丘脑外侧区域产生的心血管效应。
DOI：
10.1152/ajpheart.1989.257.2.h540
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Loewy,AD
中科院分区：
文献类型：
--
作者：
Spencer,SE;Sawyer,WB;Loewy,AD
在戊巴比妥麻醉的大鼠中，将L-谷氨酸微量注射到下丘脑外侧区（LHAt）的结节区引起血压和心率下降。心动过缓由β-肾上腺素能和毒蕈碱机制介导，如药理学阻断所示。低血压是由于心输出量减少，而不是总外周阻力减少。此外，冠状动脉血流量减少。如果通过药物阻断或电心脏起搏保持心率恒定，L-谷氨酸刺激LHAt仍会导致血压下降。当使用电起搏模型时，这种低血压是由于心输出量下降所致。相反，在心脏的药物阻断下，低血压是由于总外周阻力降低。起搏条件下的心输出量减少并非仅由药理学阻断确定的β-交感神经或副交感神经机制介导。通过药物或起搏保持心率恒定，LHAt刺激不会改变任何血管床（包括冠状动脉循环）中的局部血流或阻力。我们的结论是，L-谷氨酸刺激LHAt降低心输出量和心率的副交感神经和β-肾上腺素能机制和elevently低血压，通过降低心输出量在幼稚和电起搏模型。
L-Glutamate microinjections into the tuberal region of the lateral hypothalamic area (LHAt) caused a fall in blood pressure and heart rate in pentobarbital-anesthetized rats. The bradycardia was mediated by both beta-adrenergic and muscarinic mechanisms as demonstrated with pharmacological blockade. The hypotension was due to a decrease in cardiac output, not a decrease in total peripheral resistance. In addition, there was a reduction in coronary blood flow. If heart rate was held constant by pharmacological blockade or by electrical cardiac pacing, L-glutamate stimulation of the LHAt still caused a fall in blood pressure. When the electrically paced model was used, this hypotension was due to a fall in cardiac output. In contrast, with the pharmacological blockade of the heart, the hypotension was due to a decrease in the total peripheral resistance. The cardiac output reduction in the paced condition was not mediated solely by either beta-sympathetic or parasympathetic mechanisms as determined by pharmacological blockade. With heart rate held constant by either drugs or pacing, LHAt stimulation did not alter regional blood flow or resistance in any vascular bed, including the coronary circulation. We conclude that L-glutamate stimulation of the LHAt lowers the cardiac output and heart rate by both parasympathetic and beta-adrenergic mechanisms and elicits hypotension by lowering cardiac output in the naive and electrically paced model.