Abstract:

Objective The study is to observe the effect of nitric oxide（NO） donor and scavenger to the hypoglossal motor nucleus（HMN） activity and explore the underlying mechanism. Methods Male adult anesthetized Wistar rats were anesthetized. The activity of genioglossus（GG）, diaphragma, blood pressure（BP） and respiratory rate（RR）were recorded when constant microdialysis perfusion of artificial cerebrospinal fluid（ACSF） to HMN as control, followed with diethylamine NONOate sodium salt hydrate（DEA）, a NO donor, and 2-（4-carboxyphenyl）-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt（carboxy-PTIO）, a NO scavenger. Results Compared with ACSF, application of DEA and carboxy-PTIO at HMN increased and decreased the GG activity respectively and significantly（P<0.05）, mainly respiratory-related activity. The tonic GG, diaphragma activity, BP and RR had not been affected statistically between 30-120 min when microdialysis perfusion of both DEA and carboxy-PTIO were delivered. Conclusion Acting as an excitatory neurotransmitter of HMN, NO may contribute to the patency of upper airway physiologically.

Key words: nitric oxide, hypoglossal motor nucleus, neurotransmitter, genioglossus, obstructive sleep apneahypopnea syndrome