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Effect of low-level vagus nerve stimulation on atrialfibrillation induced by obstructive sleep apnea in dogs |
MENG Qingjun ZHANG Ling Jiasuoer·Xiaokereti WANG Xuesheng ZHOU Xianhui TANG Baopeng▲ |
Department of Cardiology, the First Affiliated Hospital of Xinjiang Medical University, Xinjiang Uygur Autonomous Region, Urumqi 830054, China |
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Abstract Objective To investigate the mechanism of low-level vagus nerve stimulation (LL-VNS) in the treatment of atrial fibrillation (AF) induced by obstructive sleep apnea (OSA) in dogs. Methods Eighteen adult male healthy beagle dogs were randomly divided into three groups:control group (n = 6),OSA group (n = 6) and OSA + LL-VNS group (n = 6). All animals were intubated under general anesthesia. Both the OSA group and the LL-VNS group performed the same OSA process,which was suffocated for 2 min, ventilated for 8 min, and 10 min was a cycle lasting 6 h. The OSA + LL-VNS group was given LL-VNS from the third hour to the end of the experiment and the control group was not suffocated. The changes of blood gas indexes at 0, 1, 3 h, and 6 h, and inflammatory markers including tumor necrosis factor-α (TNF-α), interleukin-2 (IL-2) and interleukin-6 (IL-6) at 0, 3 h and 6 h after modeling were detected. The canine arterial blood pressure was recorded throughout the whole experiment. At the end of the experiment, the atrial muscle tissue was taken for hematoxylin-eosin (HE) staining. Results OSA model was successfully established (P < 0.05). The systolic blood pressure of OSA group and OSA + LL-VNS group had significantly changed before and after OSA (P < 0.05), but there was no significant difference between the two groups (P > 0.05). Inflammation indicators-TNF-α, IL-2 at 6 hours in OSA group were significantly higher than the control group, but in OSA + LL-VNS group, it was significantly lower than the control group, the differences were statistically significant (P < 0.05). IL-6 showed no significant change in each time period (P > 0.05). In OSA group the atrial relative refractory period (ERP) was gradually shortened, and AF duration was gradually prolonged (P < 0.05). In OSA + LL-VNS group, from 0 h to 3 h the atrial ERP was gradually shortened and the duration of AF was gradually prolonged (P < 0.05); from 3 h to 6 h after given LL-VNS, the atrial ERP was gradually extended and AF duration reduced compared with 0 h to 3 h (P < 0.05). Compared with the control group, the HE slices of the atrial muscle in the OSA group showed that the atrial myocytes were disordered and the cell gap widened and After LL-VNS intervention, the above changes were reversed to some extent. Conclusion Inflammatory factors are positively correlated with the genesis and development of AF, and LL-VNS can reduce the incidence of AF. Therefore, reducing the body's inflammatory response may be one of the mechanisms by which LL-VNS reduces AF inducibility.
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