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Introduction Although the precise cause of obstructive sleep apnea (OSA) remains unknown, various anatomical or structural factors are thought to influence upper airway patency. Recent clinical studies show that OSA is frequently observed among patients with fluid‐retaining states, such as heart/renal failure and postsurgery. It is important to note that a cause–effect relationship is not yet established, and our understanding of the effects of fluid overload is limited. The goal of this study was to investigate an animal model that can characterize the physiological changes that occur in response to fluid overload. Method Acute nonsurvival experiments were conducted in 16 Sprague–Dawley rats. Rats were initially anesthetized by inhaled isoflurane, while the femoral vein was cannulated and urethane (1.2–1.5 g/Kg body weight) was gradually delivered intravenously to induce anesthesia. Additional doses of urethane were delivered as necessary to maintain a surgical plane of anesthesia. A surgical incision was made on the cervical area to catheterize carotid artery to measure blood pressure. A pair of stainless‐steel wires was injected into the tongue to measure genioglossus muscle activity (GGEMG). All physiological measurements were recorded as intravenous infusion of saline was provided to the rat (infusion rate = 22 ml/kg over 30 min). Results Acute saline overloading resulted in a 33% decrease in GGEMG, when compared to baseline. There was also a gradual drop in the respiratory rate (13% decrease) that reached statistical significance at 10 min after infusion was stopped. The blood pressure exhibited a 14% increase which subsequently returned to baseline within 40 min stopping infusion. There were no significant changes in the heart rate. Conclusion The results of this study indicate that systemic fluid overload can affect significant changes in different physiological systems including reduction in genioglossus muscle activity, increase in blood pressure, and change autonomic nervous system function., In this study, the effects of acute intravenous saline infusion on multiple physiological parameters—such as respiratory, cardiovascular, and autonomic nervous system—which was conducted in urethane anesthetized rodents were evaluated. Our results showed that “fluid overloading” causes a significant decrease in upper airway dilator muscle activity, which is a characteristic biomarker observed in obstructive sleep apnea patients.

Overnight extracellular rostral fluid shifts have been shown to be of importance in patients with fluid-retaining states and are associated with a higher prevalence of sleep apnea. Pulmonary hypertension is frequently associated with right ventricular dysfunction and progressive right ventricular failure, and an increased prevalence of sleep apnea has been described. In light of the importance of fluid shifts in the pathophysiology of sleep apnea, we aimed to explore temporal fluid shifts in patients with pulmonary hypertension with and without sleep apnea. Patients with pulmonary hypertension (WHO Group 1 or 4) had overnight extracellular rostral fluid shift assessment before and a minimum of 3 months after initiation of pulmonary hypertension-specific therapy. Fluid shift measurements of extracellular leg, abdominal, thoracic and neck fluid volumes were performed simultaneously. Twenty-nine patients with pulmonary hypertension (age 55 ± 16 years, 69% female) participated. Sleep apnea was diagnosed in 15 subjects (apnea-hypopnea index 14 [8-27] per hr). There were no significant differences in baseline or overnight leg extracellular rostral fluid, abdominal extracellular rostral fluid, thoracic extracellular rostral fluid or neck extracellular rostral fluid between those with and without sleep apnea. There was a significant inverse correlation between the sleep apnea severity and the overnight change in leg extracellular rostral fluid (r = -0.375, p = 0.049). There were no significant differences detected in overnight extracellular rostral fluid shifts from baseline to follow-up. Treatment-naïve patients with pulmonary hypertension both with and without sleep apnea demonstrate overnight extracellular rostral fluid shifts from the legs into the thorax and neck. Pulmonary hypertension-specific treatment, while significantly improving cardiac haemodynamics, had little impact on nocturnal extracellular rostral fluid shifts or the presence of sleep apnea.