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低氧血症时听神经-脑干诱发电位的抑制——作用机制及部位

The depression of the auditory nerve-brain-stem evoked response in hypoxaemia--mechanism and site of effect.

作者信息

Sohmer H, Freeman S, Gafni M, Goitein K

出版信息

Electroencephalogr Clin Neurophysiol. 1986 Oct;64(4):334-8. doi: 10.1016/0013-4694(86)90157-4.

Abstract

During severe hypoxaemia in the cat the ABR was depressed in 2 different patterns: if mean arterial blood pressure (MAP) was maintained then all other evoked potentials (EPs--somatosensory and visual) remained. If MAP was not maintained, all of these EPs were depressed. This study sought to document these different patterns of ABR depression and to ascertain their mechanisms. When MAP fell, the ABR loss began with the later waves and progressed to the earlier waves. These are signs of a central brain lesion. The hypoxaemia, detrimental to normal function of the cardiovascular system, leads to depression of MAP, to a fall in cerebral perfusion pressure and blood flow, to cerebral ischaemia and ABR loss. On the other hand, when MAP was maintained, severe hypoxaemia was accompanied by a depression of all of the ABR waves at the same time. The cochlear microphonic potential was also simultaneously depressed. These are signs of a peripheral, cochlear effect similar to the demonstrated depression of the positive endocochlear resting potential of the scala media and of the cochlear microphonic potential during hypoxaemia. This leads to interference with the cochlear transduction mechanism so that all of the auditory evoked potentials, including the ABR, are simultaneously depressed. These results lead to the suggestion that the ABR abnormalities seen in patients who suffered a hypoxic (anoxic) insult or an ischaemic episode (prolonged interpeak latencies, loss of later waves and finally all waves absent or only the first wave remaining) is always due to ischaemia even when the initial insult was hypoxic.

摘要

在猫发生严重低氧血症时,听觉脑干反应(ABR)以两种不同模式受到抑制:如果平均动脉血压(MAP)得以维持,那么所有其他诱发电位(EPs——体感诱发电位和视觉诱发电位)仍保持正常。如果MAP未得到维持,所有这些诱发电位都会受到抑制。本研究旨在记录ABR抑制的这些不同模式并确定其机制。当MAP下降时,ABR波幅降低始于较晚出现的波,并逐渐发展至较早出现的波。这些是中枢脑损伤的迹象。低氧血症对心血管系统的正常功能有害,导致MAP降低、脑灌注压和血流量下降、脑缺血以及ABR波幅降低。另一方面,当MAP得以维持时,严重低氧血症会同时伴有所有ABR波的波幅降低。耳蜗微音器电位也会同时受到抑制。这些是外周耳蜗效应的迹象,类似于低氧血症期间所证实的蜗管中内淋巴静息电位正值和耳蜗微音器电位降低。这会干扰耳蜗的换能机制,从而使包括ABR在内的所有听觉诱发电位同时受到抑制。这些结果表明,在遭受缺氧(无氧)损伤或缺血发作(峰间期延长、较晚出现的波幅降低,最终所有波消失或仅余第一波)的患者中所见的ABR异常总是由缺血所致,即使最初的损伤是缺氧性的。

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