| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1990: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1989: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Research Abstract |
Although the importance of the vagal nerve in the pathogenesis of bronchial asthma has been reported, its precise contribution is still not fully understood. To shed more light on this area, we performed the following experiments.
First, we evaluated the possible contribution of vagal reflex in Histamine-Induced Bronchoconstriction (HIB), and decided the site of action of histamine on the vagal nerve. For this purpose, we studied the effects of the bilateral cervical vagotomy, hexamethonium (2 mg/kg) or tetrodotox in (0.5 mg/kg) on HIB (8 mug/kg, iv) in anesthetized and mechanically ventilated guinea pigs. We also studied whether or not atropine (1 mg/kg) decreases HIB after vagotomy, including either the treatment of hexamethonium or tetrodotoxin.
The following results were obtained ; 1) The response to histamine was significantly enhanced by the vagotomy, hexamethonium or tetrodotoxin. 2) Propranolol increased HIB and HIB was further enhanced by the vagotomy in the animals treated with
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propranolol. 3) Atropine significantly suppressed HIB after the vagotomy, hexamethonium or tetrodotoxin. These results suggest that the postganglionic vagus nerve plays an excitatory role in HIB through the release of acetylcholine from the nerve terminals. It is also suggested that the vagal reflex mainly exhibits an inhibitory role in the HIB of guinea pigs, presumably by the
Second, to elucidate whether the local reflex may release tachykinin, we studied the effects of atropine (10^<-6> M), tetrodotoxin (TTX) (10^<-7> M) on the bradykinin induced contraction of guinea pig Tracheal Smooth Muscle (TSM) in vitro, with or without capsaicin pretreatment. Atropine did not change the contraction induced by bradykinin in the control animals. TTX suppressed bradykinin-induced contraction. Neither atropine nor TTX did affect bradykinin-induced contraction of TSM in the animals with capsaicin pretreatment.
These results indicated that bradykinin may cause a local neurally mediated action in TSM contraction, without release of acetylcholine from efferent vagal nerve terminals, presumably by the release of tachykinins from vagal efferent endings through axon reflex. Less
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