Premium
Role of Reactive Oxygen Species in Intermittent Hypoxia Induced Sympathoexcitation
Author(s) -
Eubank Wendy L,
White Daniel,
Moralez Gilbert,
Kay Victoria,
Watenpaugh Donald E,
Raven Peter B
Publication year - 2013
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.27.1_supplement.938.2
Subject(s) - medicine , oxidative stress , hypoxia (environmental) , nitric oxide , reactive oxygen species , anesthesia , acetylcysteine , endocrinology , blood pressure , pathogenesis , oxygen , chemistry , antioxidant , biochemistry , organic chemistry
The mechanism by which OSA affects the cardiovascular system remains unknown. In healthy adults, acute intermittent hypoxic apnea (IHA) is associated with a sustained increase in muscle sympathetic nerve activity (MSNA) with and without changes in mean arterial pressure (MAP). Centrally generated oxidative stress is implicated in the pathogenesis of OSA. It is probable that the increases in central sympathetic outflow (CSO) are centrally generated reactive oxygen species (CROS) mediated by CROS scavenging the central nitric oxide (CNO) which dampens CSO. To investigate the role of CROS in IHA induced sympathoexcitation. We tested the hypothesis that pretreatment with N‐Acetyl Cysteine (NAC) will completely suppress the IHA induced increase in CROS and blunt the increase in CSO following 20 min of IHA. In 5 healthy adults, age 40 ± 19 yrs, ht 180 ± 14 cm, wt 89 ± 14 kg muscle sympathetic nerve activity (MSNA) was recorded from the peroneal nerve prior to during and following a 20 minute IHA induction of sympathoexcitation following oral ingestion of 7mg/Kg of N‐Acetylcysteine (NAC). Total MSNA was not significantly different pre‐ to post‐IHA with pretreatment of NAC (2539.274 ± 489.981 au Pre‐IHA and 2728.709 ± 727.913 au Post‐IHA). We conclude that NAC pretreatment attenuated the previously demonstrated elevation in total MSNA and burst frequency after intermittent hypoxia. NIH Grant # HL106431