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突触前神经递质以及对自然刺激的化学感应反应。

Presynaptic neurotransmitter and chemosensory responses to natural stimuli.

作者信息

Pokorski M, Lahiri S

出版信息

J Appl Physiol Respir Environ Exerc Physiol. 1984 Feb;56(2):447-53. doi: 10.1152/jappl.1984.56.2.447.

Abstract

We investigated the hypothesis that release of acetylcholine from presynaptic nerve terminals in the carotid body may be responsible for the excitation of carotid body chemoreceptors by hypoxia and hypercapnia and central ventilatory stimulation by hypercapnia. 4-Aminopyridine, an agent known to release presynaptic transmitters including acetylcholine, was administered intravenously (1 mg X kg-1) or by close intra-arterial injection to the carotid body (200 micrograms) in anesthetized cats. 4-Aminopyridine did not change the carotid chemosensory responses to any arterial PO2 or PCO2 levels studied, whereas it stimulated ventilation at all arterial PO2 and PCO2 levels. Atropine blocked the ventilatory effects of 4-aminopyridine but not the responses to hypoxia and hypercapnia. The results add to the evidence, which shows that the presynaptic cholinergic mechanism is not germane to carotid body chemoreception. Also, acetylcholine does not seem to mediate the central hypercapnic stimulation of ventilation.

摘要

我们研究了这样一种假说

颈动脉体中突触前神经末梢释放乙酰胆碱可能是低氧和高碳酸血症激发颈动脉体化学感受器以及高碳酸血症引起中枢性通气刺激的原因。4-氨基吡啶是一种已知可释放包括乙酰胆碱在内的突触前递质的药物,将其静脉注射(1毫克/千克)或通过颈动脉体动脉内近距离注射(200微克)给予麻醉猫。4-氨基吡啶并未改变所研究的颈动脉化学感受反应对任何动脉血氧分压或二氧化碳分压水平的影响,然而它在所有动脉血氧分压和二氧化碳分压水平下均刺激通气。阿托品阻断了4-氨基吡啶的通气效应,但未阻断对低氧和高碳酸血症的反应。这些结果进一步证明,突触前胆碱能机制与颈动脉体化学感受无关。此外,乙酰胆碱似乎并未介导高碳酸血症对通气的中枢性刺激作用。

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