Neurologic Examination for Anesthesiologists: Reply.
Neurologic Examination for Anesthesiologists: Reply.
复制标题
麻醉师神经系统检查：答复。
DOI：
10.1097/aln.0000000000002913
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发表时间：
2019
期刊：
影响因子：
8.8
通讯作者：
Brown,EmeryN
中科院分区：
文献类型：
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作者：
Brown,EmeryN
Drummond教授提出了一个很好的观点，即异丙酚引起的呼吸暂停并不完全是通过其作用于γ-氨基丁酸介导的神经质和脑桥的背侧和腹侧呼吸群突触而发生的。然而，他进一步写道：“我认为，在这种情况下，意识丧失是由唤醒中枢的抑制所介导的，Reshef等人也认为这是更可能导致呼吸暂停的原因。”在有意识的受试者中，呼吸通常不是由化学传感器刺激维持的，而是由意识本身维持的……静脉注射一剂后，意识丧失通常会导致呼吸暂停，因为在短时间内没有其他刺激来提供呼吸驱动。”这些陈述并没有提供任何关于意识丧失如何“导致”呼吸暂停的具体电路机制。极有可能的是，大量服用异丙酚会导致脑干中γ-氨基丁酸介导的抑制优势。正如我们之前所指出的，在大量服用异丙酚后，脑干部分的意识丧失，很可能是由于其作用于γ-氨基丁酸介导的从下丘脑视前区到觉醒中心的投射。2-4此外，脑干中存在广泛的γ-氨基丁酸介导的回路，因此当异丙酚等药物作为丸剂给予时，它会不加区分地作用于所有这些回路，提供无数种使呼吸中枢失活的可能性。γ-氨基丁酸介导的脑干失活机制与呼吸暂停之间的关系需要更多的研究。我们同意，大剂量服用异丙酚导致呼吸暂停与吸入诱导不同，在吸入诱导中，患者变得无意识，但可以继续呼吸。研究支持
Professor Drummond makes a good point that apnea induced by propofol does not occur entirely through its actions at γ-aminobutyric acid–mediated synapses in the dorsal and ventral respiratory groups in the medulla and pons. However, he further writes,“I suggest that loss of consciousness mediated by suppression of the arousal centers, which is also considered by Reshef et al., 1 to be a more likely cause of apnea in these circumstances. In conscious subjects, respiration is generally sustained not by chemosensor stimulation, but by consciousness itself… After a bolus of IV agent, loss of consciousness often causes apnea, because there is, for a short time, no alternative stimulus to provide respiratory drive.” These statements do not offer any specific circuit mechanism as to how loss of consciousness “causes” apnea. What is highly plausible is that bolus administration of propofol leads to a preponderance of γ-aminobutyric acid–mediated inhibition in the brainstem. As we have pointed out previously, the brainstem component of loss of consciousness following bolus administration of propofol, is due most likely to its actions at the γ-aminobutyric acid–mediated projections from the preoptic area of the hypothalamus on to the arousal centers. 2–4 In addition, there is extensive γ-aminobutyric acid–mediated circuitry in the brainstem such that when an agent like propofol is administered as a bolus, it acts indiscriminately at all of these circuits, offering a myriad of possibilities to inactivate the respiratory centers. 5–7 More work is needed to trace out precisely the relationship between brainstem inactivation due to γ-aminobutyric acid–mediated mechanisms and apnea. We agree that bolus administration of propofol leading to apnea is different from an inhalational induction in which the patient becomes unconscious but can continue to breath. research Support