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清醒大鼠对窒息的通气反应:环境温度和体温的影响

Ventilatory response to asphyxia in conscious rats: effect of ambient and body temperatures.

作者信息

Mortola J P, Maskrey M

机构信息

Department of Anatomy and Physiology, University of Tasmania at Hobart, Australia.

出版信息

Respir Physiol. 1998 Mar;111(3):233-46. doi: 10.1016/s0034-5687(98)00003-6.

DOI:10.1016/s0034-5687(98)00003-6
PMID:9628229
Abstract

In many mammals the ventilatory response to hypoxia depends on ambient temperature (Ta), largely because of the hypometabolic effects of hypoxia below thermoneutrality. We questioned whether the ventilatory response to asphyxia also depends upon Ta, and the role played by metabolism and body temperature (Tb). Oxygen consumption (VO2) and pulmonary ventilation (VE) were measured in conscious rats at Ta = 27 degrees C (warm) and 11 degrees C (cold), breathing air or two levels of asphyxic gases, moderate (10% O2-4% CO2), or severe (10% O2-8% CO2), for approximately 30 min each. In the cold, the pattern of the VE response to moderate asphyxia was qualitatively similar to that seen in hypoxia alone, i.e the attained VE/VO2 was similar in warm and cold conditions, with, in the latter, a major drop in VO2 and little or no hyperpnea. During severe asphyxia, however, the VE/VO2 attained in the cold was less than in the warm, and it was accompanied by a large drop in Tb (approximately 6 degrees C). Blood gases confirmed the lower asphyxic hyperventilation in the cold. By maintaining Tb at 38 degrees C with an implanted abdominal heat exchanger, the VE/VO2 levels attained during asphyxia were the same between cold and warm conditions. We conclude that (a) the VE response to asphyxia is Ta-dependent, largely because of the hypometabolic effect of the hypoxic component in the cold, (b) during moderate asphyxia the hypercapnic component is qualitatively unimportant, and (c) with severe asphyxia the hypercapnia becomes an important contributor to the Ta-sensitivity by aggravating the decrease in Tb in the cold and lowering VE sensitivity.

摘要

在许多哺乳动物中,对低氧的通气反应取决于环境温度(Ta),这主要是因为低于热中性温度时低氧具有低代谢效应。我们质疑对窒息的通气反应是否也取决于Ta,以及代谢和体温(Tb)所起的作用。在清醒大鼠中,于Ta = 27摄氏度(温暖)和11摄氏度(寒冷)条件下测量耗氧量(VO2)和肺通气量(VE),大鼠呼吸空气或两种窒息气体水平,即中度(10% O2 - 4% CO2)或重度(10% O2 - 8% CO2),每种情况持续约30分钟。在寒冷环境中,对中度窒息的VE反应模式在质量上与单独低氧时相似,即在温暖和寒冷条件下达到的VE/VO2相似,在寒冷条件下,VO2大幅下降,几乎没有或没有呼吸增强。然而,在重度窒息期间,寒冷环境中达到的VE/VO2低于温暖环境,并且伴随着Tb大幅下降(约6摄氏度)。血气分析证实寒冷环境中窒息性过度通气较低。通过植入腹部热交换器将Tb维持在38摄氏度,寒冷和温暖条件下窒息期间达到的VE/VO2水平相同。我们得出结论:(a)对窒息的VE反应取决于Ta,这主要是因为寒冷中低氧成分的低代谢效应;(b)在中度窒息期间,高碳酸血症成分在质量上不重要;(c)在重度窒息时,高碳酸血症通过加剧寒冷中Tb的下降和降低VE敏感性,成为Ta敏感性的重要促成因素。

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