We have previously reported that bedtime ethanol (2.0 ml/kg of 100 proof vodka) increases upper airway closing pressure in males who habitually snored but were otherwise healthy. We also observed that some of these snorers developed obstructive apneas. To explore this phenomenon in more detail, we measured the inspiratory resistance (R 1 ) and respiratory drive after bedtime ethanol in 10 nonobese men (ages 23 to 33) with no history of snoring. Subjects went to bed wearing a tightly fitting valved mask over the nose and mouth that allowed measurement of inspiratory and expiratory flow, pressure in the mask, and endtidal CO 2 . We measured R 1 by calculating the pressure difference between the mouth and a balloon positioned in the midesophagus. Respiratory drive was quantified by the inspiratory occlusion pressure (P 0.1 ), the ventilatory response to hyperoxic hypercapnia (ΔV̇E/ΔP ET CO 2 ), and the ventilatory response to isocapnic hypoxia (ΔV̇E/ΔS a O 2 ). Measurements were made during waking and during stage 2 NREM sleep on two nights: (1) when the subjects drank 1.5 ml/kg of 100 proof vodka in orange juice over a 30-min period 15-45 min before lights out and (2) when the orange juice contained less than 0.1 ml of vodka floating on the top. Eight of the nine men in whom we had technically adequate measurements showed a rise in R 1 during NREM sleep above the waking level on both control and ethanol nights and the sleeping R 1 was greater on the ethanol than on the control night. There was a tendency for P 0.1 to be higher during sleep and greater on the ethanol night, suggesting that the neural output to the respiratory muscles was not depressed and may have been stimulated by the inspiratory "loading" secondary to the increased R 1 . The hypercapnic response was significantly depressed during sleep. Whereas the response tended to be less on the ethanol than on the control night, the difference was not significant. The hypoxic response showed little change from waking to sleeping and no significant change with ethanol. We speculate that inspiratory loading due to increased upper airway resistance tends to stimulate respiratory drive and thereby partially offsets the depressant effect of ethanol on the central respiratory chemoreceptors. Keywords Ethanol; Respiratory Drive; Sleep; Upper Airway ResistanceThe depressant effect of ethanol on respiratory drive has been recognized for many years. 1-4 More recently, we and others have shown that moderate doses of ethanol taken at bedtime can have another deleterious effect on respiration by increasing the upper airway resistance. Ethanol increases snoring in men who snore and worsens the severity of apneic episodes in patients with obstructive sleep apnea. 1,5-9 However, there are no data examining the effects of ethanol on inspiratory resistance in nonsnorers whose upper airway remains relatively patent during sleep. This study was done to characterize and analyze the magnitude of changes in inspiratory resistance and respiratory drive after a group of norm...

No abstract

No abstract