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Mechanisms of life-shrecthening attacks of asthma.

哮喘致命发作的机制。

基本信息

批准号：
09670592
负责人：
KIKUCHI Yoshihiro
金额：
$ 1.73万
依托单位：
Tohoku University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09670592/
关键词：
Bronchial asthma Death from asthma Dyspnea hypoxia beta2-stimulant inhalation β刺激剤吸入

项目摘要

The purpose of the present was to examine the precise mechanisms of death from asthma attacks. Specifically, I intended to clarify my hypothesis that an increase in physical activity and/or an inhalation of beta2-stimulant during an exerbation of asthma maybe a trigger of unconsciousness, leading to death.Main findings in this project were as follows.1. I interviewed to 28 patients with near-fatal asthma, who had in experience of unconsciousness during an attack or had received treatment with a mechanical ventilator. Sixty-eight percent of their near-fatal episodes had occurred just after the increasing physical activity, in particular walking, and 17 percent had occurred after/or during the inhalation of beta2-stimulant through an ultrasonic nebulizer. These results suggest that the increase in physical activity and the inhalation of beta2-stimulant during an exerbation of asthma may be a trigger of unconsciousness, leading to death.2 It was also demonstrated that both the increase physical activity and the inhalation of beta2-stimulant decreased in arterial oxygen saturation during an exacerbation of asthma. The more severe airway bronchoconstriction expressed by peak expiatory flow was, the more oxygen saturation decreased by an inhalation of beta2-stimulant.3. It was demonstrated that doxapram increases the perception of dyspnea during breathing through resistances as well as hypoxic ventilatory response. This suggest that doxapram may improve the two risk factors, i.e. blunted perception of dyspnea and lower edhypoxic ventilatory response, of patients with near-fatal asthma. This drug may be useful for a treatment for patients with near-fatal asthma.

本研究的目的是研究哮喘发作导致死亡的确切机制。具体而言，我打算澄清我的假设，即在哮喘发作期间增加体力活动和/或吸入β 2-兴奋剂可能是无意识的触发因素，导致死亡。本项目的主要发现如下。我采访了28名几乎致命的哮喘患者，他们在发作期间有无意识的经历或接受过机械呼吸机治疗。68%的几乎致命的事件发生在增加体力活动之后，特别是步行，17%发生在通过超声雾化器吸入β 2兴奋剂之后或期间。这些结果表明，在哮喘发作期间，体力活动的增加和β 2-兴奋剂的吸入可能是无意识的触发因素，导致死亡。2还证明，在哮喘发作期间，体力活动的增加和β 2-兴奋剂的吸入都会降低动脉血氧饱和度。吸入β 2-兴奋剂后，气道支气管收缩程度越重，血氧饱和度下降越多.研究表明，多沙普仑通过阻力和低氧性呼吸反应增加呼吸困难的感觉。这表明多沙普仑可能改善了两个危险因素，即呼吸困难感觉迟钝和缺氧缓解反应降低，几乎致命的哮喘患者。这种药物可能对治疗几乎致命的哮喘患者有用。