Mg. Persson et al., ETHANOL CAUSES DECREMENTS IN AIRWAY EXCRETION OF ENDOGENOUS NITRIC-OXIDE IN HUMANS, European journal of pharmacology. Environmental toxicology and pharmacology section, 270(4), 1994, pp. 273-278
Ethanol has previously been demonstrated to inhibit excretion of endog
enous nitric oxide (NO) in exhaled air from experimental animals. The
aim of the present study was to elucidate if this effect also occurs i
n human subjects. Healthy volunteers ingested ethanol (0.25 and 1 g kg
(-1), 20% in orange juice). Nitric oxide in exhaled air was determined
by chemiluminescence. Single-breath analysis of exhaled air was perfo
rmed and peak values of NO and end expiratory levels of NO and CO2 wer
e determined. Ethanol induced dose-dependent decrements in exhaled nit
ric oxide. Thus, peak values for nitric oxide in exhaled air, in the f
irst exhalation after breath-holding for 30 s, decreased to 56 +/- 10
and 37 +/- 12% of control 60 min after ingestion of ethanol at 0.25 an
d 1 g kg(-1) respectively. Rinsing the oral cavity (including gargling
) for 15 min with 20% ethanol in juice did not significantly influence
NO in exhaled air. Heart rate, blood pressure and end expiratory leve
ls of CO2 were not significantly affected by ethanol ingestion. In con
clusion, ethanol decreases levels of nitric oxide in exhaled air in hu
mans, likely by inhibition of airway formation of nitric oxide. The re
sults might be of importance in understanding effects of ethanol and o
ther hydrocarbons.