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氧气和二氧化碳向猴子中耳逆向扩散导致中耳压力增加。

Increases in middle ear pressure resulting from counter-diffusion of oxygen and carbon dioxide into the middle ear of monkeys.

作者信息

Doyle W J

机构信息

Department of Otolaryngology, Children's Hospital of Pittsburgh, USA.

出版信息

Acta Otolaryngol. 1997 Sep;117(5):708-13. doi: 10.3109/00016489709113464.

DOI:10.3109/00016489709113464
PMID:9349867
Abstract

The mechanism of middle ear (ME) pressure regulation is incompletely understood. Previously, Hergels and Magnuson reported an unexpected increase in ME pressure for human subjects who partially evacuated their relative positive ME pressures by swallowing. They suggested that a novel, but unknown mechanism for the generation of gas was responsible for the pressure increase. In this experiment, the MEs of rhesus monkeys were inflated with N2 via the eustachian tube and post inflation ME pressures were recorded for up to three hours. Eleven of 20 experiments showed an initial increase in ME pressure caused by the inflation followed by stable pressures for the remainder of the followup period. In 9 of the experiments, a rapid and temporally discrete decrease in ME pressure was observed during the course of followup. Following the observed pressure decrease which was interpreted as a transient eustachian tube opening, ME pressures showed a progressive increase characterized by a kinetic pattern similar to that of the human experiment. To understand the mechanism responsible for this effect, the monkey experiment was simulated using a mathematical model of ME pressure regulation. Free parameters of the model were taken from experimental data for monkeys. The model accurately predicted the time course of pressure change documented in the monkey experiments. The effect is driven by a decrease in the preexisting ME partial pressures of CO2, O2 and H2O consequent to tubal openings at relative positive pressures, with the subsequent counter diffusion of those gases from blood to ME causing the observed increase in total ME pressure. The results reported by Hergels and Magnuson can also be explained by this mechanism.

摘要

中耳(ME)压力调节机制尚未完全明确。此前,赫格斯和马格努森报告称,对于通过吞咽部分排出相对正性中耳压力的人类受试者,其中耳压力意外增加。他们认为,一种产生气体的新的但未知的机制导致了压力增加。在本实验中,通过咽鼓管向恒河猴的中耳注入氮气,并记录注入后长达三小时的中耳压力。20个实验中有11个显示,注入导致中耳压力最初增加,随后在随访期的剩余时间内压力稳定。在9个实验中,随访过程中观察到中耳压力迅速且在时间上离散性下降。在观察到被解释为咽鼓管短暂开放的压力下降之后,中耳压力呈现出逐渐增加的趋势,其动力学模式与人体实验相似。为了解释这种效应的机制,使用中耳压力调节的数学模型模拟了猴子实验。模型的自由参数取自猴子的实验数据。该模型准确预测了猴子实验中记录的压力变化时间进程。这种效应是由相对正压时咽鼓管开放导致中耳预先存在的二氧化碳、氧气和水蒸气分压降低所驱动的,随后这些气体从血液反向扩散到中耳,导致观察到的中耳总压力增加。赫格斯和马格努森报告的结果也可以用这种机制来解释。

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Ann Otol Rhinol Laryngol. 2007 Jan;116(1):69-75. doi: 10.1177/000348940711600112.