EFFECTS OF NITROGLYCERIN AND SODIUM-NITROPRUSSIDE ON ENDEXPIRATORY CONCENTRATIONS OF NITRIC-OXIDE IN HEALTHY HUMANS

The cellular origin of nitric oxide (NO) in exhaled air of healthy hum ans is unknown. It is currently not known, whether changes in NO conce ntrations that originate from pulmonary vessels, can be detected as ch anges in exhaled NO. Thus, we have studied the effects of increased in travascular NO generation on endexpiratory NO-levels. Twenty-four youn g healthy volunteers received nitroglycerin (GTN), sodium nitroprussid e (SNP) or placebo iv. in a randomized, double blind cross-over trial. Diastolic blood pressure decreased from 59 mmHg (95% confidence inter val: 56-62) during placebo to 48 mmHg (CI: 45-51) and to 48 mmHg (CI: 45-50) after infusions of GTN and SNP, respectively. Heart rate increa sed from 69 (CI: 65-73) during placebo to 78 (CI: 72-84) and to 84 (CI : 77-92) after infusions of GTN and SNP, respectively (p<0.01 for all comparisons). However, no increase in exhaled NO was detected: endexpi ratory NO-concentrations averaged 6.1 ppb (CI: 4.9-7.4), 5.7 ppb (CI: 4.4-7.0) and 6.4 ppb (CI: 5.3-7.6) under placebo, GTN and SNP infusion s, respectively (Friedman ANOVA p=0.328). NO release from within the p ulmonary vasculature does not significantly contribute to endexpirator y NO concentrations in non-intubated healthy humans suggesting that su ch NO measurements quantify NO production mainly from non-vascular pul monary cells. (C) 1998 Elsevier Science Inc.