Respiratory Physiology & Neurobiology 185 (2013) 489–496 Contents lists available at SciVerse ScienceDirect Respiratory Physiology & Neurobiology j our nal ho me p age: www.elsevier.com/locate/resphysiol Resetting the baroreflex during snoring: Role of resistive loading and intra-thoracic pressure Jyotishna Narayan a,b,c,∗ , Jason Amatoury a,b,c , Manisha Verma a,b , Kristina Kairaitis a,b,c , John R. Wheatley a,b,c , Terence C. Amis a,b,c a Ludwig Engel Centre for Respiratory Research, Australia b Westmead Millennium Institute, Westmead, Australia c University of Sydney at Westmead Hospital, Westmead, Sydney, NSW, Australia a r t i c l e i n f o Article history: Accepted 19 November 2012 Keywords: Snoring Negative intrathoracic pressure Baroreflex sensitivity a b s t r a c t Baroreflex sensitivity (BRS) is reduced during snoring in humans and animal models. We utilised our rabbit model to examine the contribution of increased upper airway resistance to baroreflex resetting during snoring, by comparing BRS and baroreflex operating point (OP) values during IS to those obtained during tracheostomised breathing through an external resistive load (RL) titrated to match IS levels of peak inspiratory pleural pressure (Ppl). During both IS and RL, BRS decreased by 45% and 49%. There was a linear relationship between the change in Ppl and the decrease in BRS, which was similar for IS and RL. During both RL and IS, there was a shift in OP driven by ∼16% increase in HR and no change in arterial pressure. Snoring related depression of BRS is likely mediated via a HR driven change in OP, which itself may be the outcome of negative intra-thoracic pressure mediated effects on right atrial wall stretch reflex control of heart rate. © 2012 Elsevier B.V. All rights reserved. 1. Introduction The arterial baroreflex is a pressure sensing, negative feedback control system that modulates short-term beat-to-beat regulation of arterial blood pressure. The sensitivity of this homeostatic con- trol system is defined in terms of the slope of the relationship between arterial blood pressure and heart rate. Sleep-wake state influences BRS such that, in healthy subjects, values measured dur- ing sleep tend to be higher than those recorded during wakefulness (Conway et al., 1983; Legramante et al., 2003; Lombardi and Parati, 2000; Vaile et al., 1996; Van de Borne et al., 1994). However, the opposite is the case when subjects experience sleep disordered breathing (SDB), with a number of studies documenting lower BRS values during sleep in patients with obstructive sleep apnoea (OSA) (Carlson et al., 1996; Gates et al., 2004; Mateika et al., 1999; Parati et al., 1997; Ryan et al., 2007). OSA is characterised by snoring with recurrent apnoeas and hypopnoeas, frequently accompanied by episodes of hypoxaemia (Dempsey et al., 2010; White, 2006). The mechanistic linkage ∗ Corresponding author at: Ludwig Engel Centre for Respiratory Research, Depart- ment of Respiratory and Sleep Medicine, Cnr of Darcy and Hawkesbury Rd, Westmead Hospital, Westmead, Sydney, NSW2145, Australia. Tel.: +61 2 9845 7366; fax: +61 2 9845 7286. E-mail address: jyotishna.narayan@sydney.edu.au (J. Narayan). between these nocturnal SDB events and reduced BRS remains unclear, but sympathetic surges commonly associated with apnoeic events (Carlson et al., 1993, 1996; Levinson and Millman, 1991; Somers et al., 1995) and/or chemoreceptor activation, particu- larly in response to hypoxaemia (Dunai et al., 1999; Levinson and Millman, 1991; Polo et al., 1991; Prabhakar et al., 2005, 2007; Shahar et al., 2001; Somers et al., 1989) are most commonly pro- posed. Reduced BRS values during sleep, however, are also known to occur during periods of non-hypoxic snoring (Mateika et al., 1999), suggesting linkages between SDB and BRS that do not depend on the presence of hypoxaemia or occurrence of the sympathetic activation associated with apneic events. Recently, we described a non-hypoxic, non-apneic, anaesthetised rabbit model in which external compression of the pharyngeal airway is used to increase upper airway resistance and induce snoring (Narayan et al., 2012). In this model, induced snoring led to ∼40% fall in BRS and a change in BRS operating point (prevailing heart rate and blood pressure) characterised by an increase in heart rate but no significant change in blood pressure. In the present study we examine the contribution of increased upper airway resistance to baroreflex resetting during snoring by comparing BRS and operating point values obtained dur- ing induced snoring in anaesthetised rabbits (intact upper airway) with those obtained during tracheostomised breathing through an external resistive load titrated to match induced snoring levels of peak inspiratory intra-pleural pressure (Ppl). 1569-9048/$ – see front matter © 2012 Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.resp.2012.11.011