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INHIBITION OF CLONIDINE ON PRE‐INSPIRATORY ACTIVITY OF THE UPPER AIRWAY MOTOR NERVES IN THE RAT
Author(s) -
Chen Yifan,
Lee KunZe,
Tsai ChihYi,
Tsai HsinYeh,
Lu IJung,
Hwang JiChuu
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.lb126
Subject(s) - clonidine , medicine , airway , anesthesia , agonist , phrenic nerve , apnea , hypoglossal nerve , respiratory system , receptor , tongue , pathology
Clonidine is an agonist of the α 2 ‐adrenergic receptor and a common drug used for the treatment of hypertention. It has been documented that clonidine produces a decrease in respiratory frequency and also induction of obstructive sleep apnea. We thus hypothesized that clonidine might modulate activity of the upper airway motor nerves. Activities of the phrenic nerve (PN), recurrent laryngeal nerve (RLN) and hypoglossal nerve (HN) were simultaneously recorded in anesthetized and ventilated Wistar rats. The data we obtained showed that intra‐jugular administration of clonidine (2.5, 5, or 10 μg/kg) produced a dose‐dependent depression of the pre‐inspiratory activities of the RLN and HN, which was abolished by pretreatment of blockade of the α 2 ‐adrenergic receptor. These data suggest that activation of the α 2 ‐adrenergic receptor may participate in the modulation of upper airway patency by inhibiting the pre‐inspiratory activity of the upper airway motor nerves.