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Patients with OSA have compromised upper airway anatomy making the airway more vulnerable to collapse (76-80). During wakefulness, reflex mechanisms lead to increased upper airway dilator muscle activity keeping the collapsible part of the upper airway open (79,81). However, with sleep onset, these reflex mechanisms are lost resulting in a fall in upper airway dilator muscle activity, and upper airway collapse in those anatomically susceptible (82). A variety of respiratory stimulants have been used to increase upper airway muscle activity during sleep in an attempt to treat patients with sleep apnea. Thus far, the results have been disappointing and no drug can currently be recommended.

The prevalence of sleep apnea increases after menopause, suggesting that female hormones may play a protective effect on sleep-disordered breathing (83). Medroxyprogesterone (Cycrin®, Provera®) is a respiratory stimulant and has been used to treat OSA by increasing central neural drive to the pharyngeal muscles. Strohl et al. (84) demonstrated improvement in 4/9 patients with OSA in an uncontrolled study; of note, three of the four subjects who improved were hypercapnic suggesting that they may have had an element of obesity-hypoventilation syndrome in addition to OSA. Subsequent studies, however, have not been as impressive, with mild to no improvement of OSA after treatment with progesterone (85,86), even in postmenopausal women (87). Furthermore, the combined use of estrogen and progesterone does not appear to be effective (88).

At this time, progesterone cannot be considered an effective treatment for OSA, though it may play an adjunctive role in patients with the obesity-hypoventilation syndrome by its effects on central respiratory drive. However, the potential procoagulant effects of progesterone should be considered, especially given the high doses required and their increased risk of thromboembolic and cardiovascular disease (89).

Protriptyline (Vivactil®), a tricyclic antidepressant, has also been proposed as a treatment of OSA (90). Overall, protriptyline may modestly decrease the AHI and degree of oxygen desaturation. Though protriptyline may increase genioglossus tone (perhaps through its anticholinergic effect), the predominant mechanism is likely through its suppression of REM sleep (the stage of sleep during which OSA is usually the most severe). This drug has a variety of side effects including urinary retention, dry mouth, and impotence. Therefore, although this drug may be a reasonable option in patients with mild, predominately REM-associated OSA, the drug is often poorly tolerated due to the myriad of adverse side effects.

Other respiratory stimulants such as nicotine, theophylline (Theolair®, Uniphyl®), acetazolamide (Diamox®), naloxone (Narcan®), almitrine, and bromocriptine (Parlodel®) are also not useful in treating OSA (91-93). Serotonergic drugs are described in more detail subsequently.

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