Spencer S E, Sawyer W B, Loewy A D
Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63110.
Am J Physiol. 1989 Aug;257(2 Pt 2):H540-52. doi: 10.1152/ajpheart.1989.257.2.H540.
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.
向戊巴比妥麻醉的大鼠下丘脑外侧区结节部（LHAt）微量注射L-谷氨酸会导致血压和心率下降。药理学阻断实验表明，心动过缓是由β-肾上腺素能和毒蕈碱能机制共同介导的。低血压是由于心输出量减少，而非总外周阻力降低。此外，冠状动脉血流量也会减少。如果通过药理学阻断或心脏电起搏使心率保持恒定，L-谷氨酸对LHAt的刺激仍会导致血压下降。使用心脏电起搏模型时，这种低血压是由于心输出量下降所致。相比之下，在对心脏进行药理学阻断时，低血压是由于总外周阻力降低所致。药理学阻断实验表明，在起搏状态下的心输出量减少并非仅由β-交感神经或副交感神经机制介导。无论是通过药物还是起搏使心率保持恒定，刺激LHAt均不会改变任何血管床（包括冠状动脉循环）的局部血流量或阻力。我们得出结论，L-谷氨酸对LHAt的刺激通过副交感神经和β-肾上腺素能机制降低心输出量和心率，并在未处理和心脏电起搏模型中通过降低心输出量引发低血压。
