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异丙肾上腺素诱发呼吸急促的机制。

Mechanisms of hyperpnea induced by isoproterenol.

作者信息

Eldridge F L, Gill-Kumar P

出版信息

Respir Physiol. 1980 Jun;40(3):349-63. doi: 10.1016/0034-5687(80)90034-1.

DOI:10.1016/0034-5687(80)90034-1
PMID:7444220
Abstract

We injected boluses of isoproterenol (2 to 3 micrograms) into the inferior vena cava to determine the effects on phrenic activity, end-tidal PCO2, arterial pressure and aortic flow in anesthetized cerebrate and unanesthetized decerebrate cats. We studied both spontaneously breathing animals and those paralyzed and servo-ventilated to keep end-tidal PCO2 constant. Isoproterenol caused an increase of respiratory output within a few seconds if carotid bodies were intact; recordings of the carotid sinus nerves showed that the response was due to activation of carotid body chemoreceptors. After denervation of both carotid bodies isoproterenol still caused a late (approximately 16 sec) but smaller increase of respiratory output, which persisted after section of vagi and thoracic (T1-5) dorsal roots. We concluded that the major effect of isoproterenol on respiration is through its excitatory action on the carotid bodies. There is another small, late facilitatory effect, of uncertain mechanism but not caused by peripheral chemoreceptors, by other receptors in the heart and lungs or by a change in PaCO2 acting on the central chemoreceptors.

摘要

我们将异丙肾上腺素大剂量(2至3微克)注入下腔静脉,以确定其对麻醉的有脑动物和未麻醉的去脑猫的膈神经活动、呼气末二氧化碳分压、动脉血压和主动脉血流量的影响。我们研究了自主呼吸的动物以及那些瘫痪并通过伺服通气以保持呼气末二氧化碳分压恒定的动物。如果颈动脉体完整,异丙肾上腺素会在几秒钟内导致呼吸输出增加;颈动脉窦神经的记录表明,这种反应是由于颈动脉体化学感受器的激活。在双侧颈动脉体去神经支配后,异丙肾上腺素仍会导致呼吸输出出现延迟(约16秒)但幅度较小的增加,这种增加在切断迷走神经和胸段(T1 - 5)背根后仍然持续。我们得出结论,异丙肾上腺素对呼吸的主要作用是通过其对颈动脉体的兴奋作用。还有另一种较小的、延迟的促进作用,其机制尚不确定,并非由外周化学感受器、心脏和肺部的其他受体或作用于中枢化学感受器的动脉血二氧化碳分压变化引起。

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Mechanisms of hyperpnea induced by isoproterenol.异丙肾上腺素诱发呼吸急促的机制。
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Thorax. 1995 Feb;50(2):139-42. doi: 10.1136/thx.50.2.139.
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Pflugers Arch. 1983 Mar;396(4):269-76. doi: 10.1007/BF01063930.
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J Physiol. 1987 Dec;393:43-55. doi: 10.1113/jphysiol.1987.sp016809.
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