Changes In Obstructive Sleep Apnea Research Articles

Neuroendocrine changes in sleep apnea

To review recent investigations examining the effects of neuroendocrine changes in obstructive sleep apnea. Gonadal hormones have long been implicated in the pathogenesis of obstructive sleep apnea. Recently, exogenous testosterone has been shown to exacerbate obstructive sleep apnea, whereas hormone replacement therapy in menopausal women may be protective in obstructive sleep apnea. Effective treatment of obstructive sleep apnea with nasal continuous positive airway pressure has been associated with improved insulin sensitivity and testicular function in individuals with obstructive sleep apnea. It is important to consider the potential development of sleep apnea in any patient who has an endocrine disorder or is receiving certain hormonal therapies. Effective assessment and management of obstructive sleep apnea with nasal continuous positive airway pressure may lead to a reduction in insulin resistance and hypertension as well as other markers of vascular risk in patients with metabolic syndrome.

Upper airway muscle inflammation and denervation changes in obstructive sleep apnea.

Inflammatory cell infiltration and afferent neuropathy have been shown in the upper airway (UA) mucosa of subjects with obstructive sleep apnea (OSA). We hypothesized that inflammatory and denervation changes also involve the muscular layer of the pharynx in OSA. Morphometric analysis was performed on UA tissue from nonsnoring control subjects (n = 7) and patients with OSA (n = 11) following palatal surgery. As compared with control subjects, inflammatory cells were increased in the muscular layer of patients with OSA, with CD4+ and activated CD25+ T cells (both increased approximately threefold) predominating. Inflammation was also present in UA mucosa, but with a different pattern consisting of CD8+ (2.8-fold increase) and activated CD25+ (3.2-fold increase) T cell predominance. As ascertained by immunoreactivity for the panneuronal marker PGP9.5, there was a dramatic (5.7-fold) increase in intramuscular nerve fibers in OSA patients compared with control subjects, as well as direct evidence of denervation based on positive immunostaining of the muscle fiber sarcolemmal membrane for the neural cell adhesion molecule in patients with OSA. These data suggest that inflammatory cell infiltration and denervation changes affect not only the mucosa, but also the UA muscle of patients with OSA. This may have important implications for the ability to generate adequate muscular dilating forces during sleep.

Electron beam CT airway changes in obstructive sleep apnea

Electron beam CT airway changes in obstructive sleep apnea

The Relationship Between Endothelin-1 and Blood Pressure Changes in Obstructive Sleep Apnea

The Relationship Between Endothelin-1 and Blood Pressure Changes in Obstructive Sleep Apnea

The relationship between endothelin-1 and blood pressure changes in obstructive sleep apnea

The relationship between endothelin-1 and blood pressure changes in obstructive sleep apnea

Impairment of cerebral perfusion during obstructive sleep apneas.

Cerebral circulation was studied in six patients with obstructive sleep apnea (OSA) by transcranial Doppler. Cerebral blood flow velocity (CBFV), pulsatility index (Pi), intra-arterial radial blood pressure, transcutaneous blood gases, and respiration were recorded during sleep with or without apneas. There was a concomitant increase of mean arterial pressure (Pa) and CBFV by 11 +/- 6% (p < 0.001) and 15 +/- 6% (p < 0.001) compared with baseline at 5.1 +/- 2.4 and 5.3 +/- 2.6 s, respectively, after apnea termination. Pa and CBFV decreased to a minimum of -8 +/- 2% (p < 0.001) and -23 +/- 8% (p < 0.001), respectively, below baseline at 19.8 +/- 5.0 and 19.4 +/- 4.5 s after apnea. Values returned to baseline within 60 s, except during repetitive apneas, which were associated with prolonged periods of reduced Pa and CBFV. Pi changed inversely to CBFV and rose to 34 +/- 15% (p < 0.001) above baseline 19.5 +/- 5.5 s after the end of apnea because of a decrease in diastolic CBFV. There was a close correlation between Pa and CBFV (r = 0.67, p < 0.001), indicating that cerebral autoregulation is insufficient to protect the brain from rapid systemic pressure changes in OSA. The findings suggest that apneas during sleep are associated with profound changes in cerebral blood flow. Apnea-induced hypoxemia combined with reduced cerebral perfusion may predispose to nocturnal cerebral ischemia in patients with OSA.