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Mechamisms of death from asthma-basic and clinical approach-

哮喘死亡机制——基本和临床方法——

基本信息

批准号：
07670649
负责人：
KIKUCH Yoshihiro
金额：
$ 1.6万
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：
1995
资助国家：
日本
起止时间：
1995 至 1996
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07670649/
关键词：
Brnchial asthma death from asthma hypoxia Dyspnea Carotid body Posithon emission tomography Positron emission tomography

项目摘要

We have recently reported that patients with near-fatal asthma have lowered hypoxic respiratory response as well as blunted perception of dyspnea, suggesting that these two factors are predisposing factors to death from asthma attacks. We speculate that these factors may be due to dysfunction of peripheral (carotid) chemoreceptors. In this study, we have examined the relationships among death from asthma, hypoxic respiratory responses and the function of carotid body.Our results were as follows,(1) Using positron emission tomography, we have demonstrated that cingulate cortex, thalamus and premoter cortex were activated during inspiratory resistive loaded breathing in healthy subjects and that these areas were less activated in patients with nearfatal asthma.(2) We have found expression of C-fos oncogen in the cingulate cortex, thalamus, hypothalamus, and pons of rats, which were exposed to hypoxia, hypercapnia or inspiratory resistance by using in situ hybridization and immunohistochemistry.. These results suggest that these area of the brain may be involved in the genesis of dyspnea and/or behavioral control of breathing during loaded breathing.(3) The effects of doxapram on dyspnea and ventilatory response to hypoxia were examined in 7 normal subjects. Doxapram increased dyspnea snsation as well as hypoxic ventilatory response. There was a relationship dyspnea and the ablity of hypoxic ventilatory response, suggesting that carotid chemoreceptor may play some role in the genesis of dyspnea sensation.

我们最近报道，濒临致命的哮喘患者的缺氧呼吸反应降低，呼吸困难的感觉减弱，表明这两个因素是哮喘发作死亡的诱发因素。我们推测这些因素可能是由于外周（颈动脉）化学感受器功能障碍所致。在这项研究中，我们研究了哮喘死亡、缺氧呼吸反应和颈动脉体功能之间的关系。我们的结果如下：（1）使用正电子发射断层扫描，我们证明健康受试者的扣带皮层、丘脑和前运动皮层在吸气阻力负荷呼吸期间被激活，而在近乎致命的哮喘患者中这些区域的激活程度较低。（2）我们发现采用原位杂交和免疫组织化学方法，采用原位杂交和免疫组织化学方法，研究了缺氧、高碳酸血症或吸气阻力大鼠的扣带皮层、丘脑、下丘脑和脑桥中C-fos癌基因的表达。这些结果表明，大脑的这些区域可能参与了负荷呼吸期间呼吸困难和/或呼吸行为控制的发生。(3) 在 7 名正常受试者中检查了多沙普仑对缺氧呼吸困难和通气反应的影响。多沙普仑增加呼吸困难以及缺氧通气反应。呼吸困难与缺氧通气反应能力存在相关性，提示颈动脉化学感受器可能在呼吸困难感的发生过程中发挥一定作用。