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大鼠防御反应的神经效应机制

Neuroeffector mechanisms of the defense reaction in the rat.

作者信息

Carobrez A P, Schenberg L C, Graeff F G

出版信息

Physiol Behav. 1983 Oct;31(4):439-44. doi: 10.1016/0031-9384(83)90063-x.

DOI:10.1016/0031-9384(83)90063-x
PMID:6657764
Abstract

Electrical stimulation of the dorsal periaqueductal gray matter (DPAG) eliciting flight behavior in awake rats caused an increase in arterial blood pressure (BP), heart rate (HR) and respiration in rats anesthetized with urethane. The hypertension was markedly reduced by 5 mg/kg of intravenously injected hexamethonium or bretylium, virtually abolished by 5 mg/kg of phentolamine and partially antagonized by 0.1 mg/kg of the alpha 1-adrenoceptor blocker, prazosin. The tachycardia induced by DPAG stimulation was partially antagonized by hexamethonium or bretylium and abolished by propranolol (5 mg/kg, IV) or practolol (5 mg/kg, IV), but not affected by N-butylscopolamine (10 mg/kg, IV). Phentolamine increased basal HR and abolished the tachycardic response caused by either brain stimulation or intravenous noradrenaline. Prazosin moderately decreased the response to noradrenaline, but did not affect basal HR or the tachycardia induced by brain stimulation. The increase in respiratory amplitude occurring during brain stimulation was abolished by phentolamine as well as by prazosin, while the increase in respiratory rate was moderately reduced by phentolamine and propranolol. These results demonstrate that the cardiovascular component of the defense reaction of the rat is almost entirely due to a sharp increase in sympathetic tone. They also suggest that the hyperventilation induced by aversive brain stimulation is modulated by central and peripheral adrenergic mechanisms.

摘要

对清醒大鼠中脑导水管周围灰质背侧(DPAG)进行电刺激引发逃避行为时,会导致用乌拉坦麻醉的大鼠动脉血压(BP)、心率(HR)和呼吸增加。静脉注射5mg/kg六甲铵或溴苄铵可使高血压明显减轻,5mg/kg酚妥拉明可几乎完全消除高血压,而0.1mg/kg的α1肾上腺素能受体阻滞剂哌唑嗪可部分拮抗高血压。六甲铵或溴苄铵可部分拮抗DPAG刺激引起的心动过速,普萘洛尔(5mg/kg,静脉注射)或普拉洛尔(5mg/kg,静脉注射)可消除心动过速,但N-丁基东莨菪碱(10mg/kg,静脉注射)对其无影响。酚妥拉明可增加基础心率,并消除脑刺激或静脉注射去甲肾上腺素引起的心动过速反应。哌唑嗪可适度降低对去甲肾上腺素的反应,但不影响基础心率或脑刺激引起的心动过速。酚妥拉明和哌唑嗪均可消除脑刺激期间出现的呼吸幅度增加,而酚妥拉明和普萘洛尔可适度降低呼吸频率增加。这些结果表明,大鼠防御反应的心血管成分几乎完全是由于交感神经张力急剧增加所致。它们还表明,厌恶脑刺激引起的过度通气受中枢和外周肾上腺素能机制调节。

相似文献

1
Neuroeffector mechanisms of the defense reaction in the rat.大鼠防御反应的神经效应机制
Physiol Behav. 1983 Oct;31(4):439-44. doi: 10.1016/0031-9384(83)90063-x.
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GABA modulation of the defense reaction induced by brain electrical stimulation.γ-氨基丁酸对脑电刺激诱发的防御反应的调节作用
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Depressant action of chlordiazepoxide on cardiovascular and respiratory changes induced by aversive electrical stimulation of the brain.氯氮䓬对脑厌恶电刺激诱发的心血管和呼吸变化的抑制作用。
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Cardiovascular change in response to prolonged defense area stimulation in freely moving rats.自由活动大鼠长时间防御区刺激后心血管系统的变化。
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Dorsal periaqueductal gray post-stimulation freezing is counteracted by neurokinin-1 receptor antagonism in the central nucleus of the amygdala in rats.大鼠杏仁核中央核中神经激肽-1受体拮抗作用可抵消导水管周围灰质背侧刺激后引起的僵住反应。
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Effects of clonidine, prazosin and phentolamine on heart rate and coronary sinus catecholamine concentration during cardioaccelerator nerve stimulation in spinal dogs.可乐定、哌唑嗪和酚妥拉明对脊髓麻醉犬心脏加速神经刺激期间心率和冠状窦儿茶酚胺浓度的影响。
Br J Pharmacol. 1979 Oct;67(2):283-92. doi: 10.1111/j.1476-5381.1979.tb08678.x.

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