PT  - JOURNAL ARTICLE
AU  - DH Yates
AU  - SA Kharitonov
AU  - RA Robbins
AU  - PS Thomas
AU  - PJ Barnes
TI  - The effect of alcohol ingestion on exhaled nitric oxide
AID  - 10.1183/09031936.96.09061130
DP  - 1996 Jun 01
TA  - European Respiratory Journal
PG  - 1130--1133
VI  - 9
IP  - 6
4099  - http://erj.ersjournals.com/content/9/6/1130.short
4100  - http://erj.ersjournals.com/content/9/6/1130.full
SO  - Eur Respir J1996 Jun 01; 9
AB  - The concentration of nitric oxide (NO) is increased in the exhaled air of patients with inflammatory lung diseases, including asthma, possibly reflecting cytokine-mediated chronic airway inflammation. Endogenous NO is generated from L-arginine by the action of several types of NO synthase (NOS). NOS have structural similarities with cytochrome P450 reductases. Alcohol decreases exhaled NO in animals, but this has not previously been investigated in man. We studied the effect of alcohol ingestion in nine asthmatic and 12 normal subjects, measuring the peak concentration of exhaled NO using a modified chemiluminescence analyser. A significant decrement in NO occurred in asthmatic patients (mean +/- SEM before ethanol 204 +/- 58 to 158 +/- 59 parts per billion (ppb) after ethanol; p < 0.02), without significant change in the normal subjects (122 +/- 14 to 114 +/- 15 ppb). Thus, in our study, alcohol decreased exhaled nitric oxide in asthmatic subjects but not in normal individuals. This may reflect preferential action on inducible nitric oxide synthase which is expressed in asthmatic airways. An inhibitory effect of ethanol on inducible nitric oxide synthase may contribute towards the effect of alcohol in asthma.