REDUCED ENDOGENOUS NITRIC-OXIDE IN THE EXHALED AIR OF SMOKERS AND HYPERTENSIVES

We wanted to determine whether the production of endogenous nitric oxi de (NO) is affected by cigarette smoking and various pathological cond itions. Endogenously produced NO was measured by chemiluminescence in the exhaled air of 81 healthy volunteers (21 nonsmoking females (NSF), 12 smoking females (SF), 24 nonsmoking males (NSM) and 24 smoking mal es (SM)) and 38 patients (10 with hypertension, 10 intra- and 10 posto perative, 5 with renal failure and 3 with sepsis) entered the protocol . Subjects inspired from a NO-free air supply, which was also used to calibrate the NO-analyser. Endogenous NO production of volunteers was 18+/-8 per billion (ppb) depending on smoking habits. In exhaled air o f NSF, NO concentration was 21+/-7 ppb, in SF 16+/-6 ppb, in NSM 19+/- 8 ppb and in SM 15+/-6 ppb. Differences between smokers and nonsmokers were significant. Increased diastolic blood pressure was noted in SM compared to NSM (86+/-7 versus 78+/-7 mmHg). Patients with documented and treated hypertension (systolic and diastolic blood pressure: 141+/ -18 and 82+/-9 mmHg) exhaled 13.7+/-5.3 ppb NO; hypertensive males 10/-2 ppb NO and females 17+/-5 ppb NO. In patients with renal failure N O concentration in exhaled air was 20.2+/-6.8 ppb before and 19.8+/-6. 4 ppb one hour after the onset of dialysis. In patients under going ma jor surgery NO concentration was 5.6+/-2.5 ppb intra- and 10.3+/-3.5 p pb postoperatively. In three mechanically ventilated patients with doc umented septic syndrome, exhaled NO was 29.3+/-24 ppb. We conclude tha t smokers and patients with hypertension exhale significantly less NO than healthy volunteers. This suggests that exhaled NO can be used as a mark er and therapeutic target in disease.