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布洛芬阻断大鼠低氧通气的时间依赖性增加。

Ibuprofen blocks time-dependent increases in hypoxic ventilation in rats.

机构信息

Division of Physiology, Department of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0623, United States.

出版信息

Respir Physiol Neurobiol. 2011 Sep 30;178(3):381-6. doi: 10.1016/j.resp.2011.03.024. Epub 2011 Mar 30.

DOI:10.1016/j.resp.2011.03.024
PMID:21457799
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3158279/
Abstract

Recently, inflammatory processes have been shown to increase O(2)-sensitivity of the carotid body during chronic sustained hypoxia [Liu, X., He, L., Stensaas, L., Dinger, B., Fidone, S., 2009. Adaptation to chronic hypoxia involves immune cell invasion and increased expression of inflammatory cytokines in rat carotid body. Am. J. Physiol. Lung Cell Mol. Physiol. 296, L158-L166]. We hypothesized that blocking inflammation with ibuprofen would reduce ventilatory acclimatization to hypoxia by blocking such increases in carotid body O(2) sensitivity. We tested this in conscious rats treated with ibuprofen (4mg/kg IP daily) or saline during acclimatization to hypoxia ( [Formula: see text] for 7 days). Ibuprofen blocked the increase in hypoxic ventilation observed in chronically hypoxic rats treated with saline; ibuprofen had no effects on ventilation in normoxic control rats. Ibuprofen blocked increases in inflammatory cytokines (IL-1β, IL-6) in the brainstem with chronic hypoxia. The data supports our hypothesis and further analysis indicates that ibuprofen also blocks inflammatory processes in the central nervous system contributing to ventilatory acclimatization to hypoxia. Possible mechanisms linking inflammatory and hypoxic signaling are reviewed.

摘要

最近的研究表明,在慢性持续低氧期间,炎症过程会增加颈动脉体对 O(2)的敏感性[Liu, X., He, L., Stensaas, L., Dinger, B., Fidone, S., 2009. 适应慢性低氧涉及免疫细胞浸润和大鼠颈动脉体中炎症细胞因子表达增加。美国生理学杂志。肺细胞分子生理学 296, L158-L166]。我们假设,通过阻断炎症反应,使用布洛芬(ibuprofen)阻断颈动脉体 O(2)敏感性的增加,从而减少低氧通气适应。我们在接受布洛芬(4mg/kg IP 每日)或生理盐水治疗的清醒大鼠中对此进行了测试,这些大鼠在低氧环境中适应([Formula: see text]持续 7 天)。布洛芬阻断了慢性低氧生理盐水治疗大鼠中观察到的低氧通气增加;布洛芬对正常氧对照大鼠的通气没有影响。布洛芬阻断了慢性低氧下脑干部位炎症细胞因子(IL-1β、IL-6)的增加。这些数据支持我们的假设,进一步的分析表明,布洛芬还阻断了中枢神经系统中的炎症过程,从而促进了低氧通气适应。综述了可能将炎症和低氧信号联系起来的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab90/3158279/62600ad5d442/nihms285597f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab90/3158279/fc96b37c5568/nihms285597f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab90/3158279/ccd30a623fd5/nihms285597f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab90/3158279/62600ad5d442/nihms285597f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab90/3158279/fc96b37c5568/nihms285597f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab90/3158279/ccd30a623fd5/nihms285597f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab90/3158279/62600ad5d442/nihms285597f3.jpg

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