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高压惊厥发作中的时间、速率和温度因素。

Time, rate, and temperature factors in the onset of high-pressure convulsions.

作者信息

Brauer R W, Beaver R W, Lahser S, Mansfield W M, Sheehan M E

出版信息

J Appl Physiol Respir Environ Exerc Physiol. 1977 Aug;43(2):173-82. doi: 10.1152/jappl.1977.43.2.173.

Abstract

An interrupted compression profile technique was used to develop data to separate the effects of time and pressure factors governing increase of high-pressure neurological syndrome (HPNS) convulsion threshold pressures (the compression rate effect) during different compression profiles. A single differential equation fits all data available to date for compression rate effect on convulsion thresholds of CD-1 mice (three distinct types of compression profile; mean compression rates 12-1,000 atm/h). The process leading to increase in HPNS convulsion pressure is initiated at the very beginning of compression, proceeds at increasingly rapid rates as higher pressures are attained, and approaches a limiting upper convulsion pressure. The convulsion threshold pressure in any given experiment is independent of the compression rate prevailing during the time immediately preceding onset of the seizure. The magnitude of the compression rate effect in the CD-1 mouse is independent of chamber temperature over a range of 27-36 degrees C, and rectal temperatures of 29.2-37.5 degrees C. The bearing of these results on the design of optimal compression schedules and on the analysis of the neurological mechanisms underlying the HPNS is discussed.

摘要

采用间断加压模式技术来获取数据,以区分在不同加压模式下,时间和压力因素对高压神经综合征(HPNS)惊厥阈值压力升高(即加压速率效应)的影响。一个单一的微分方程适用于迄今为止所有关于CD-1小鼠惊厥阈值的加压速率效应的数据(三种不同类型的加压模式;平均加压速率为12 - 1000 atm/h)。导致HPNS惊厥压力升高的过程在加压一开始就启动,随着压力升高,速率越来越快,并趋近于一个极限惊厥压力上限。在任何给定实验中,惊厥阈值压力与发作前即刻的加压速率无关。在27 - 36摄氏度的环境温度范围以及29.2 - 37.5摄氏度的直肠温度范围内,CD-1小鼠的加压速率效应大小与环境温度无关。讨论了这些结果对优化加压方案设计以及对HPNS潜在神经机制分析的意义。

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