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Effects of acute intermittent hypoxia on sympathetic and expiratory activities in rats (872.8)
Author(s) -
Lemes Eduardo,
Bassi Mirian,
Colombari Débora,
Colombari Eduardo,
Zoccal Daniel
Publication year - 2014
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.28.1_supplement.872.8
Subject(s) - medicine , anesthesia , intermittent hypoxia , respiratory system , phrenic nerve , hypoxia (environmental) , sympathetic activity , sympathetic nervous system , cardiology , blood pressure , heart rate , chemistry , oxygen , organic chemistry , obstructive sleep apnea
The exposure to acute intermittent hypoxia (AIH) produces a long‐lasting increase of phrenic and sympathetic activities in anesthetized rats. In the present study we aimed to evaluate the effects of AIH on baseline expiratory motor activity as well as the role of retrotrapezoid nucleus in the AIH‐induced sympathetic and respiratory changes. In the in situ working heart‐brainstem preparations of juvenile rats (n=4), AIH exposure (10 x 5‐7% O2 for 30 s, every 5 min) increased baseline phrenic (Δ: 20±6%), abdominal (Δ: 65±30%) and sympathetic (Δ: 89±48%) nerve activities (P<0.05) that was maintained for at least 60 min after the last hypoxic episode. In conscious adult rats (n=9), AIH evoked an increase in baseline arterial pressure (Δ: 7±2 mmHg), associated with enhanced sympathetic‐ and respiratory‐related variabilities (P<0.05). In adult urethane‐anesthetized rats with intact vagus (n=5), AIH increased baseline arterial pressure (Δ: 9±1 mmHg) and abdominal muscle contraction amplitude (Δ: 412±117%), which were reverted by pharmacological inhibition of retrotrapezoid nucleus (P<0.05). These data indicate that AIH promotes a sustained increase of expiratory activity, in addition to inspiratory and sympathetic activities. Moreover, AIH‐induced sympathetic and expiratory long‐term facilitation may involve, at least in part, the activation of the retrotrapezoid nucleus. Grant Funding Source : Supported by FAPESP (09/54888‐7; 11/20040‐1) and CNPq