| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1996: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1995: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Research Abstract |
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.
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