Abstract
Objective:Obesity has reached epidemic proportions and is a strong risk factor for obstructive sleep apnea (OSA). However, the underlying mechanisms are poorly understood and current treatment strategies for OSA and obesity have critical limitations. Thus, establishment of an obesity-related large animal model with spontaneous OSA is imperative.Materials and methods:Natural and sedated sleep were monitored and characterized in 4 obese (body mass index - BMI>48) and 3 non-obese (BMI<40) minipigs. These minipigs were instrumented with the BioRadio system under sedation for the wireless recording of respiratory airflow, snoring, abdominal and chest respiratory movements, electroencephalogram, electrooclulogram, electromyogram, and oxygen saturation. After instrumentation, the minipigs were placed in a dark room with a remote night-vision camera for monitoring all behaviors. Wakefulness and different sleep stages were classified, and episodes of apneas and/or hypopneas were identified during natural and/or sedated sleep.Results:No hypopnea episodes were observed in two of the non-obese minipigs, but one non-obese minipig had 5 hypopnea events. Heavy snoring and 27-58 apnea and/or hypopnea episodes were identified in all 4 obese minipigs. Most of these episodes occurred in the rapid eye movement stage during natural sleep and/or sedated sleep in Yucatan minipigs.Conclusions:Obese minipigs can experience naturally occurring OSA, thus are an ideal large animal model for obese-related OSA studies.
Highlights
Obstructive sleep apnea (OSA) affects up to 20% of the population with significant morbidity and mortality, and the prevalence is increasing as obesity reaches epidemic proportions
A number of studies have indicated that obesity is a strong risk factor for OSA and changes in body weight relates to OSA severity [1]
The respiratory parameters and apnea/hypopnea index (AHI) of the same obese minipig were compared between the two monitoring sessions of natural sleep recorded on different days (4-5 days apart)
Summary
Obstructive sleep apnea (OSA) affects up to 20% of the population with significant morbidity and mortality, and the prevalence is increasing as obesity reaches epidemic proportions. A number of studies have indicated that obesity is a strong risk factor for OSA and changes in body weight relates to OSA severity [1]. Since obesity and OSA share some common mechanisms such as inflammatory activation, oxidative stress, and increased sympathetic activation, they may interact and potentiate with each other [2]. The efficacy of various treatments for OSA, including mechanical and surgical applications, experimental neuromuscular stimulation, and pharmacological interventions, are still in debate, and each treatment strategy has its critical limitations. The evaluations of treatment effectiveness are greatly limited by constraints in measuring anatomic and functional variables in humans. A validated and characterized large animal model is needed
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