PubMed1998
OBJECTIVE: In order to observe the changes of nitric oxide (NO) affected by smoking and their relationship in vivo. METHOD: 60 male nonsmoker as the control group, 192 male smoked as the study group which was divided into 4 subgroups (1-10, 11-20, 21-30 and > 30) according to the number of cigarettes smoked per day. The metabolite of nicotine-cotinine in urine was assayed by means of barbituric acid. Cotinine was used as an objective indicator to reflect the smoking quantity. The urinary NO (NO2.-) was determined with colorimetric estimation. RESULT: The urinary cotinine level in the 4 subgroups were 6.6 +/- 1.6, 25.1 +/- 6.2, 37.8 +/- 8.5, 53.6 +/- 8.3 (mumol/L) respectively. The urinary NO of nonsmokers were 4.43 +/- 0.97 (mumol/L), in the 4 subgroups it was 3.04 +/- 0.07, 2.75 +/- 0.05, 2.18 +/- 0.01, 1.60 +/- 0.01 (mumol/L) respectively. The results of statistical analysis between the 4 subgroups were t = 4.2894, P < 0.01; t = 2.7446, P < 0.01; t = 2.7667, P < 0.01 accordingly. As compared between the 4 subgroups of smokers and the nonsmokers, the statistical results were t = 2.7118, P < 0.01; t = 3.1826, P < 0.01; t = 3.2100, P < 0.01; t = 4.6600, P < 0.01; respectively. The statistical differences between the 4 subgroups were t = 2.9286, P < 0.01; t = 3.0357, P < 0.01; t = 3.8181, P < 0.01; t = 2.2160, P < 0.05 respectively. There was a good positive correlation between the number of cigarette smoked and urinary cotinine content (r = 0.8626, P < 0.01), also a significant negative correlation between it and urinary NO level (r = -0.6596, P < 0.05). A negative correlation could be observed between urinary cotinine and NO (r = -0.6026, P < 0.05). CONCLUSION: With the increase of quantity and duration of smoking, the NO content in vivo will decrease, suggested that the vascular endothelial cells could be damaged severely.