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Role of mechanoreceptive reflex activation of the genioglossus muscle in the atenuation of inspiratory flow reduction associated with negative effort dependence

Grant number: 11/22117-1
Support Opportunities:Scholarships abroad - Research
Start date: July 16, 2012
End date: July 15, 2013
Field of knowledge:Health Sciences - Medicine - Medical Clinics
Principal Investigator:Pedro Rodrigues Genta
Grantee:Pedro Rodrigues Genta
Host Investigator: Atul Malhotra
Host Institution: Instituto do Coração Professor Euryclides de Jesus Zerbini (INCOR). Hospital das Clínicas da Faculdade de Medicina da USP (HCFMUSP). Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil
Institution abroad: Harvard University, Cambridge, United States  

Abstract

Obstructive sleep apnea (OSA) is highly prevalent among adults and is associated with significant morbidity and mortality. Airflow limitation is commonly observed among OSA patients and is defined as a steady inspiratory flow despite an increasing inspiratory effort. A Starling Resistor model is often used to study the relationship between pressure and flow of the pharynx. This model considers that inspiratory flow remains constant during airflow limitation, independently of inspiratory effort. Neverthelless, negative effort dependence (NED) is a well known phenomenon in which airflow actually decreases during a flow limitation regimen, and can contribute significantly to the impairment of inspiratory airflow in OSA. However, the mechanisms associated with NED are not completely known. The purpose of this study is to evaluate the pattern of upper airway muscle (genioglossus) activity and the development of NED during flow limited breaths of OSA patients during sleep. Our hypothesis is that upper airway mechanoreceptor reflexes may protect against NED. The attenuation of phasic genioglossus activity can be achieved by topical anesthesia of the pharynx. Thus, we also hypothesize that patients with Starling Resistor type behavior (constant inspiratory flow over a range of driving pressures) will develop NED once the reflexes have been impaired with topical anesthetic. We intend to determine NED through the induction of inspiratory flow limitation by the abrupt reduction of CPAP for a few minutes, with and without topical anesthesia of the pharynx, and simultaneously monitor genioglossus muscle activity of 20 OSA patients. (AU)

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