F
Francois M. Abboud
Researcher at University of Iowa
Publications - 319
Citations - 22939
Francois M. Abboud is an academic researcher from University of Iowa. The author has contributed to research in topics: Baroreceptor & Blood pressure. The author has an hindex of 76, co-authored 319 publications receiving 21862 citations. Previous affiliations of Francois M. Abboud include Marquette University & American Heart Association.
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Journal ArticleDOI
Sympathetic neural mechanisms in obstructive sleep apnea.
TL;DR: It is concluded that patients with obstructive sleep apnea have high sympathetic activity when awake, with further increases in blood pressure and sympathetic activity during sleep, which are attenuated by treatment with CPAP.
Journal ArticleDOI
Sympathetic-Nerve Activity during Sleep in Normal Subjects
TL;DR: REM sleep is associated with profound sympathetic activation in normal subjects, possibly linked to changes in muscle tone and the hemodynamic and sympathetic changes during REM sleep could play a part in triggering ischemic events in patients with vascular disease.
Journal ArticleDOI
Relationship Between Spectral Components of Cardiovascular Variabilities and Direct Measures of Muscle Sympathetic Nerve Activity in Humans
Massimo Pagani,Nicola Montano,Alberto Porta,Alberto Malliani,Francois M. Abboud,Clay Birkett,Virend K. Somers +6 more
TL;DR: There is a predominance in the LF oscillation of blood pressure, RR interval, and sympathetic nerve activity during sympathetic activation in normal humans and during sympathetic inhibition, the HF component of cardiovascular variability predominates.
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Contrasting effects of hypoxia and hypercapnia on ventilation and sympathetic activity in humans
TL;DR: Combined hypoxia and hypercapnia have a synergistic effect on SNA as well as on VE, which concludes that HC causes greater increases in VE and SNA than does Hypoxia.
Journal Article
The effect of dietary sodium chloride on blood pressure, body fluids, electrolytes, renal function, and serum lipids of normotensive man.
TL;DR: These studies indicate that normal man is able to compensate for large differences in sodium intake with minor metabolic changes, and that hypertension might result should the sodium load not be excreted, the circulating volume become too great for the excretory capacity, or if neural or endocrine adjustments be inadequate.