دورية أكاديمية

Mechanisms by which spinal cord stimulation intervenes in atrial fibrillation: The involvement of the endothelin-1 and nerve growth factor/p75NTR pathways

التفاصيل البيبلوغرافية
العنوان: Mechanisms by which spinal cord stimulation intervenes in atrial fibrillation: The involvement of the endothelin-1 and nerve growth factor/p75NTR pathways
المؤلفون: Peng Yiyan, Li Peng, Hu Wei, Shao Qi, Li Panpan, Wen Haiyue
المصدر: Open Medicine, Vol 18, Iss 1, Pp 2955-68 (2023)
بيانات النشر: De Gruyter, 2023.
سنة النشر: 2023
المجموعة: LCC:Medicine
مصطلحات موضوعية: atrial fibrillation, spinal cord stimulation, autonomic nerves, nerve growth factor, endothelin-1, nf-kb p65, p75ntr, Medicine
الوصف: Can the spinal cord stimulation (SCS) regulate the autonomic nerves through the endothelin-1 (ET-1) and nerve growth factor (NGF)/p75NTR pathways and thus inhibit the occurrence of atrial fibrillation (AF)? In our research, 16 beagles were randomly divided into a rapid atrial pacing (RAP) group (n = 8) and a RAP + SCS group (n = 8), and the effective refractory period (ERP), ERP dispersion, AF induction rate, and AF vulnerability window (WOV) at baseline, 6 h of RAP, 6 h of RAP + SCS were measured. The atrial tissue was then taken for immunohistochemical analysis to determine the localization of ET-1, NGF, p75NTR, NF-kB p65, and other genes. Our results showed that SCS attenuated the shortening of ERP in all parts caused by RAP, and after 6 h of SCS, the probability of AF in dogs was reduced compared with that in the RAP group. Moreover, the expression of ET-1, NGF, and p75NTR in the atrial tissues of dogs in the RAP + SCS group was significantly increased, but the expression of NF-kB p65 was reduced. In conclusion, SCS promotes the positive remodeling of cardiac autonomic nerves by weakening NFκB p65-dependent pathways to interfere with the ET-1 and NGF/p75NTR pathways to resist the original negative remodeling and inhibit the occurrence of AF.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2391-5463
Relation: https://doaj.org/toc/2391-5463
DOI: 10.1515/med-2023-0802
URL الوصول: https://doaj.org/article/0aa9f914d00a40ebb0a90fcad6fd1e55
رقم الأكسشن: edsdoj.0aa9f914d00a40ebb0a90fcad6fd1e55
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:23915463
DOI:10.1515/med-2023-0802