| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1991: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1990: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Research Abstract |
1) Study of substance P release induced by immune response in the the airway tissue in vivo.
I reported that substance P is released from guinea pig bronchus as a result of immune response in vitro (1990). So, I hypothesized that this response should be induced in vivo experiment. In the study, I anesthetized guinea pigs sensitized to ovalbumin and measured the pulmonary resistance. I exposed the animals to ovalbumin to increase the pulmonary resistance, and then exposed to enkephalinase inhibitor phosphoramidon to examine whether immune response causes release of tachykinins, because tachykinins are known to be effectively cleaved by enkephalinase. Phosphoramidon significantly potentiated the increase of the pulmonary resistance induced by ovalbumin compared with the control. In contrast, phosphoramidon failed to potentiate the response in the sensitized guinea pigs which had been treated with capsaicin, which depletes tachylkinins. These results suggest that immune response causes rel
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ease of tachykinins from the guinea pig airways in vivo. (This paper is submitted to the Journal of Applied Physiology)
2) Study of drugs which inhibit release of tachykinins from unmyelinated afferent nerves.
I hypothesized that alpha and beta adrenergic stimulants, enkephalin, theophylline, and corticosteroid inhibit the release of tachykinins from the airway tissues. Because these drugs modulated the airway smooth muscle contraction, I could not measured the physiologic airway response which is induced only by the released tachykinins.
To study the releasing mechanism of tachykinins in immune response in the guinea pig bronchial tissues in vitro, I added phosphoramidon at a plateau of the contraction induced by immune response in the presence or absence of tetrodotoxin, which inhibits nerve conduction. Phosphoramidon significant potentiated the contraction, suggesting that chemical mediators released by immune response stimulat release of tathykinins by stimulating unmyelinated afferent nerve directly and not by axon reflex in the guinea pig bronchial tissues. (This paper will be presented at the 1992 American. Thoracic Society/American Lung Association International Conference in Miami Beach)
3) Study of cough inhibition by the drugs which inhibit the release of tachykinins.
Because I could not study the drugs which inhibit the release of tachykinins, this study was not done. I will do it in future by measuring tachykinins biochemically. Less
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