The aim of this paper is to reveal the change of the brain function for nicotine addicts after smoking cessation, and explore the basis of neural physiology for the nicotine addicts in the process of smoking cessation. Fourteen subjects, who have a strong dependence on nicotine, have agreed to give up smoking and insist on completing the test, and 11 volunteers were recruited as the controls. The resting state functional magnetic resonance imaging and the regional homogeneity (ReHo) algorithm have been used to study the neural activity before and after smoking cessation. A two factors mixed design was used to investigate within-group effects and between-group effects. After 2 weeks’ smoking cessation, the increased ReHo value were exhibited in the brain area of supplementary motor area, paracentral lobule, calcarine, cuneus and lingual gyrus. It suggested that the synchronization of neural activity was enhanced in these brain areas. And between-group interaction effects were appeared in supplementary motor area, paracentral lobule, precentral gyrus, postcentral gyrus, and superior frontal gyrus. The results indicate that the brain function in supplementary motor area of smoking addicts would be enhanced significantly after 2 weeks’ smoking cessation.
Objective To study the correlation between smoking and obstructive sleep apnea (OSA). Methods A total of 454 patients from October 2015 to July 2021 were retrospectively collected for nocturnal polysomnography monitoring (no less than 7 hours). The patients were divided into an OSA group (n=405) and a control group (n=49, patients with primary snoring) according to the results of polysomnography monitoring. According to the apnea hypopnea index (AHI) and the lowest oxygen saturation during sleep, the severity of OSA was classified into a mild to moderate group (5 times/h ≤ AHI<30 times/h) and a severe group (AHI ≥30 times/h). The patients were inquired about their smoking history, then the patients diagnosed with OSA were further divided into a smoking group, a smoking cessation group, and a non-smoking group based on their smoking history. Results The smoking rate of the patients in the OSA group was higher than that in the control group (50.9% vs. 32.7%, P<0.05), while the smoking rate in the severe OSA group was higher than that in the mild to moderate group (55.7% vs. 39.8%, P<0.05). Smoking was positively correlated with AHI, cumulative percentages of time spent at oxygen saturation below 90% (Ts90%), and total apnea time (r value was 0.196, 0.197, 0.163, P<0.05), while negatively correlated with the lowest and average SpO2 during sleep (r value was –0.202, –0.214, P<0.05). The logistic regression analysis with severe OSA as the outcome variable showed that smoking (OR=1.781) and obesity (OR=1.930) were independent risk factors of severe OSA (P<0.05). The comparison between groups of the OSA patients with different smoking states showed that the proportion of severe OSA, AHI, Ts90%, and total apnea time (77.8%, 53.55 times/h, 18.35%, and 111.70 minutes, respectively) of the smoking group were higher than those of the non-smoking group (62.8%, 40.20 times/h, 8.40%, and 76.20 minutes, respectively, P<0.05). The lowest SpO2 and average SpO2 during sleep (69.50%, 93.00%, respectively) of the smoking group were lower than those of the non-smoking group (75.00%, 94.00%, respectively, both P<0.05). The average SpO2 of the smoking cessation group was higher than that of the smoking group (94.00% vs. 93.00%, P<0.05), and the Ts90% of the smoking cessation group was lower than that of the smoking group (6.75% vs. 18.35%, P<0.05). Conclusions Smoking significantly affects the degree of sleep-disordered breathing and may be an independent risk factor for severe OSA. Smoking can exacerbate the severity of OSA and the degree of hypoxia, while smoking cessation can improve the degree of hypoxia in OSA patients.