Effects of nitroglycerin and sodium nitroprusside on endexpiratory concentrations of nitric oxide in healthy humans.

摘要

The cellular origin of nitric oxide (NO) in exhaled air of healthy humans is unknown. It is currently not known, whether changes in NO concentrations that originate from pulmonary vessels, can be detected as changes in exhaled NO. Thus, we have studied the effects of increased intravascular NO generation on endexpiratory NO-levels. Twenty-four young healthy volunteers received nitroglycerin (GTN), sodium nitroprusside (SNP) or placebo i.v. in a randomized, double blind cross-over trial. Diastolic blood pressure decreased from 59 mmHg (95% confidence interval: 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 increased 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: endexpiratory 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 infusions, respectively (Friedman ANOVA p=0.328). NO release from within the pulmonary vasculature does not significantly contribute to endexpiratory NO concentrations in non-intubated healthy humans suggesting that such NO measurements quantify NO production mainly from non-vascular pulmonary cells.