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Acute intermittent hypoxia induces cardiorespiratory LTF in conscious normotensive but not hypertensive rats: Dependence of vigilance states
Author(s) -
Hayward Linda F,
Castellanos Mabelin
Publication year - 2011
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.25.1_supplement.1076.13
Subject(s) - cardiorespiratory fitness , vigilance (psychology) , hypoxia (environmental) , medicine , cardiology , intermittent hypoxia , psychology , chemistry , oxygen , neuroscience , organic chemistry , obstructive sleep apnea
Recent data from anesthetized rats (Ting & Pilowsky, 2010) suggest that induction of sympathetic long‐term facilitation (sLTF) following acute intermittent hypoxia (AIH) may be more robust than respiratory LTF (rLTF). The present study evaluated whether evidence of sLTF could also be identified in conscious rats. Adult normotensive (Sprague Dawley, SD, and WKY) and hypertensive (SHR) male rats (n=6–8/group) were instrumented for sleep/wake state identification and monitoring of blood pressure (BP), heart rate (HR) and respiration. During AIH, minute ventilation (Ve), BP, and HR increased above baseline in all strains but the rise in Ve was greatest in the SD rats (~2.2 vs 1.3 x baseline). Following the offset of AIH both SD and WKY rats demonstrated evidence of rLTF during quiet wake (QW) and quiet sleep (QS) and Ve was significantly (p≤0.02) elevated above baseline (range: 1.15 to 1.26 x baseline). rLTF was paralleled by an increase in HR during QS in the SD rats (12.6±4.8, delta from baseline) and a small increase in BP during QW (WKY and SD) and QS (SD only). SHRs did not demonstrate any evidence of cardiorespiratory LTF during sleep or wake. The results of this study demonstrate that similar to rLTF, the magnitude of sLTF is both strain and state dependent. The absence of cardiorespiratory LTF in the SHR suggests that factors associated hypertension may impair cardiorespiratory plasticity.