ETHANOL CAUSES DECREMENTS IN AIRWAY EXCRETION OF ENDOGENOUS NITRIC-OXIDE IN HUMANS

Citation
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
Citations number
20
Categorie Soggetti
Pharmacology & Pharmacy",Toxicology
ISSN journal
09266917
Volume
270
Issue
4
Year of publication
1994
Pages
273 - 278
Database
ISI
SICI code
0926-6917(1994)270:4<273:ECDIAE>2.0.ZU;2-M
Abstract
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.