[Alpha 2 adrenergic control of ventilation in the rat].

D Lagneaux, J Lecomte
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Abstract

In anaesthetized rats, ventilatory stimulation induced by phentolamine, an alpha sympatholytic agent, emphasizes the role of some adrenergic mechanisms in the control of the respiratory centres activity. Phentolamine (5 and 10 mg.kg-1, iv) stimulates ventilation after a 4 s latency, tidal volume and respiratory rate being both increased. A same response can also be provoked 10 min later, by a second identical iv administration, systemic blood pressure remaining then stable at its previous low level. Hyperventilation is also observed when phentolamine is injected in totally denervated rats, without any remaining baro- or chemosensitivity. Stimulation is thus due to a central activity in relation with the release of inhibitory influences. Phentolamine also causes hyperventilation after prazosin pretreatment indicating that the alpha 1 adrenergic blockade is not involved in the post-phentolamine stimulation. This is an alpha 2 adrenergic transmission dependent mechanism. Variation of the systemic blood pressure is not the main mechanism involved in the hyperventilation induced by phentolamine. Meanwhile, baroreceptor activity modulates the central response to the drug, as shown by the negative influence of the post-vasopressin arterial hypertension. Hyperoxia is also a modulating factor acting by two ways: an inhibition of the peripheral chemoreceptors activity is added to an arterial hypertension. On the other side, activation of these chemoreceptors by almitrine bismesilate increases the respiratory responses to phentolamine. As already shown by one of us (Lagneuax, 1986), phentolamine pretreated rats are more responsive to hypoxia and to almitrine. Moreover, these phentolamine pretreated rats are protected against cardiovascular collapses and against apnea, frequently observed during hypoxia without CO2 compensation.

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[α 2肾上腺素能对大鼠通气的控制]。
在麻醉大鼠中,酚妥拉明(一种α交感神经解毒剂)诱导的通气刺激强调了一些肾上腺素能机制在控制呼吸中枢活动中的作用。酚妥拉明(5和10毫克)。Kg-1, iv)在潜伏期4 s后刺激通气,潮气量和呼吸速率均增加。同样的反应也可以在10分钟后,通过第二次相同的静脉注射引起,全身血压保持稳定在之前的低水平。在完全失神经的大鼠中注射酚妥拉明时,也观察到过度通气,没有任何剩余的气压或化学敏感性。因此,刺激是由于与抑制影响的释放有关的中枢活动。苯妥拉明也会引起哌唑嗪预处理后的过度通气,这表明α - 1肾上腺素能阻断与苯妥拉明后刺激无关。这是一种依赖α 2肾上腺素能传递的机制。全身血压的变化并不是酚妥拉明引起换气过度的主要机制。同时,压力感受器活性调节对药物的中枢反应,如抗利尿激素后动脉高血压的负面影响所示。高氧也是一种调节因子,通过两种方式起作用:抑制外周化学感受器活性增加到动脉高血压。另一方面,二甲磺酸钠激活这些化学感受器会增加对酚妥拉明的呼吸反应。正如我们其中一人(Lagneuax, 1986)已经证明的那样,经酚妥拉明预处理的大鼠对缺氧和钠碱的反应更灵敏。此外,这些经酚妥拉明预处理的大鼠可以防止心血管衰竭和呼吸暂停,在缺氧时经常观察到没有二氧化碳补偿。
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