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在窒息点处孤立缺氧会抑制有机磷中毒大鼠模型的呼吸恢复。

Respiratory recovery following organophosphate poisoning in a rat model is suppressed by isolated hypoxia at the point of apnea.

机构信息

Department of Emergency Medicine, University of Massachusetts School of Medicine, 55 Lake Ave North, Worcester, MA 01655, USA.

出版信息

Toxicology. 2012 Dec 16;302(2-3):242-7. doi: 10.1016/j.tox.2012.08.005. Epub 2012 Aug 18.

Abstract

Normal respiratory activity (eupnea) and gasping represent different types of respiratory activity, one of which is supported by oxygen (eupnea) and the other suppressed by oxygen (gasping). There is a loss of respiratory activity post-organophosphate (OP) poisoning that returns following treatment. It is not clear if post-OP respiratory activity represents eupnea or gasping. Depending on the type of respiratory activity, oxygenation during recovery from OP poisoning may have the potential to either support or suppress respiratory activity. We hypothesize that respiratory recovery following OP-induced central apnea represents a resumption of eupnea and is supported by oxygenation. We used an animal model of acute OP poisoning with detailed physiologic recordings. Animals were poisoned with dichlorvos and allowed to recover during a period of mechanical ventilation. Two experimental models were analyzed: (1) animals supported with 100% oxygen and (2) animals supported with a normoxic gas mixture titrated to a PaO(2) of 115 mmHg. Rats in this study demonstrated breathing that resumes spontaneously following OP-induced apnea with characteristics of both eupnea and gasping. The post-OP respiratory activity was suppressed by hypoxia, a characteristic of eupneic respiration and not gasping respiration. However, the respiratory rate during post-apneic breathing corresponded more closely to gasping. Analysis of phrenic nerve discharge activity was distinct from both eupnea and gasping, with peak inspiratory and post-inspiratory discharge activities significantly reduced compared to both eupnea and gasping. In summary, in this animal model post-apneic breathing distinct from eupnea and gasping that emerges following prolonged OP-induced central apnea is suppressed by hypoxia.

摘要

正常呼吸活动(平稳呼吸)和喘息代表不同类型的呼吸活动,其中一种呼吸活动得到氧气的支持(平稳呼吸),而另一种呼吸活动受到氧气的抑制(喘息)。有机磷(OP)中毒后会出现呼吸活动丧失,经治疗后恢复。目前尚不清楚 OP 中毒后呼吸活动代表平稳呼吸还是喘息。根据呼吸活动的类型,OP 中毒恢复期间的氧合作用可能具有支持或抑制呼吸活动的潜力。我们假设 OP 引起的中枢性呼吸暂停后呼吸恢复代表平稳呼吸的恢复,并得到氧合作用的支持。我们使用了有机磷中毒的动物模型进行详细的生理记录。动物用敌敌畏中毒,并在机械通气期间允许其恢复。分析了两种实验模型:(1)用 100%氧气支持的动物;(2)用调节至 115mmHg PaO2 的常氧混合气体支持的动物。本研究中的大鼠在 OP 诱导的呼吸暂停后表现出自发恢复的呼吸,具有平稳呼吸和喘息的特征。OP 中毒后呼吸活动受到缺氧的抑制,这是平稳呼吸的特征,而不是喘息呼吸的特征。然而,呼吸暂停后的呼吸频率与喘息更接近。膈神经放电活动的分析与平稳呼吸和喘息都不同,与平稳呼吸和喘息相比,吸气和吸气后放电活动的峰值明显降低。总之,在这个动物模型中,与平稳呼吸和喘息不同的是,长时间 OP 诱导的中枢性呼吸暂停后出现的呼吸暂停后呼吸受到缺氧的抑制。

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