SK4 calcium-activated potassium channels activated by sympathetic nerves enhances atrial fibrillation vulnerability in a canine model of acute stroke
Background: New-onset atrial fibrillation (AF) is common in patients with acute stroke (AS). Studies have shown that intermediate-conductance calcium-activated potassium channel channels (SK4) play an important role in cardiomyocyte automaticity. The aim of this study was to investigate the effects...
| Main Authors: | , , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2020-05-01
|
| Series: | Heliyon |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2405844020307738 |
| _version_ | 1818304680397111296 |
|---|---|
| author | Mei Yang Youcheng Wang Xiaoxing Xiong Baojun Xie Jia Liu Junkui Yin Liuliu Zi Xi Wang Yanhong Tang Congxin Huang Qingyan Zhao |
| author_facet | Mei Yang Youcheng Wang Xiaoxing Xiong Baojun Xie Jia Liu Junkui Yin Liuliu Zi Xi Wang Yanhong Tang Congxin Huang Qingyan Zhao |
| author_sort | Mei Yang |
| collection | DOAJ |
| description | Background: New-onset atrial fibrillation (AF) is common in patients with acute stroke (AS). Studies have shown that intermediate-conductance calcium-activated potassium channel channels (SK4) play an important role in cardiomyocyte automaticity. The aim of this study was to investigate the effects of SK4 on AF vulnerability in dogs with AS. Experimental: Eighteen dogs were randomly divided into a control group, AS group and left stellate ganglion ablation (LSGA) group. In the control group, dogs received craniotomy without right middle cerebral artery occlusion (MCAO). AS dogs were established using a cerebral ischemic model with right MCAO. LSGA dogs underwent MCAO, and LSGA was performed. Results: Three days later, the dispersion of the effective refractory period (dERP) and AF vulnerability in the AS group were significantly increased compared with those in the control group and LSGA group. However, no significant difference in dERP and AF vulnerability was found between the control group and the LSGA group. The SK4 inhibitor (TRAM-34) completely inhibited the inducibility of AF in AS dogs. SK4 expression and levels of noradrenaline (NE), β1-AR, p38 and c-Fos in the atrium were higher in the AS dogs than in the control group or LSGA group. However, no significant difference in SK4 expression or levels of NE, β1-AR, p38 and c-Fos in the left atrium was observed between the control group and LSGA group. Conclusion: SK4 plays a key role in AF vulnerability in a canine model with AS. The effects of LSGA on AF vulnerability were associated with the p38 signaling pathways. |
| first_indexed | 2024-12-13T06:14:33Z |
| format | Article |
| id | doaj.art-79180dfa8c35440785c4a5c43db449da |
| institution | Directory Open Access Journal |
| issn | 2405-8440 |
| language | English |
| last_indexed | 2024-12-13T06:14:33Z |
| publishDate | 2020-05-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Heliyon |
| spelling | doaj.art-79180dfa8c35440785c4a5c43db449da2022-12-21T23:57:00ZengElsevierHeliyon2405-84402020-05-0165e03928SK4 calcium-activated potassium channels activated by sympathetic nerves enhances atrial fibrillation vulnerability in a canine model of acute strokeMei Yang0Youcheng Wang1Xiaoxing Xiong2Baojun Xie3Jia Liu4Junkui Yin5Liuliu Zi6Xi Wang7Yanhong Tang8Congxin Huang9Qingyan Zhao10Department of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Cardiovascular Research Institute of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Hubei Key Laboratory of Cardiology, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR ChinaDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Cardiovascular Research Institute of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Hubei Key Laboratory of Cardiology, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR ChinaDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan City, 430060, PR ChinaDepartment of Radiology, Renmin Hospital of Wuhan University, Wuhan City, 430060, PR ChinaDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan City, 430060, PR ChinaDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Cardiovascular Research Institute of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Hubei Key Laboratory of Cardiology, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR ChinaDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Cardiovascular Research Institute of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Hubei Key Laboratory of Cardiology, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR ChinaDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Cardiovascular Research Institute of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Hubei Key Laboratory of Cardiology, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR ChinaDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Cardiovascular Research Institute of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Hubei Key Laboratory of Cardiology, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR ChinaDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Cardiovascular Research Institute of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Hubei Key Laboratory of Cardiology, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR ChinaDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Cardiovascular Research Institute of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Hubei Key Laboratory of Cardiology, 238 Jiefang Road, Wuchang, Wuhan City, 430060, PR China; Corresponding author.Background: New-onset atrial fibrillation (AF) is common in patients with acute stroke (AS). Studies have shown that intermediate-conductance calcium-activated potassium channel channels (SK4) play an important role in cardiomyocyte automaticity. The aim of this study was to investigate the effects of SK4 on AF vulnerability in dogs with AS. Experimental: Eighteen dogs were randomly divided into a control group, AS group and left stellate ganglion ablation (LSGA) group. In the control group, dogs received craniotomy without right middle cerebral artery occlusion (MCAO). AS dogs were established using a cerebral ischemic model with right MCAO. LSGA dogs underwent MCAO, and LSGA was performed. Results: Three days later, the dispersion of the effective refractory period (dERP) and AF vulnerability in the AS group were significantly increased compared with those in the control group and LSGA group. However, no significant difference in dERP and AF vulnerability was found between the control group and the LSGA group. The SK4 inhibitor (TRAM-34) completely inhibited the inducibility of AF in AS dogs. SK4 expression and levels of noradrenaline (NE), β1-AR, p38 and c-Fos in the atrium were higher in the AS dogs than in the control group or LSGA group. However, no significant difference in SK4 expression or levels of NE, β1-AR, p38 and c-Fos in the left atrium was observed between the control group and LSGA group. Conclusion: SK4 plays a key role in AF vulnerability in a canine model with AS. The effects of LSGA on AF vulnerability were associated with the p38 signaling pathways.http://www.sciencedirect.com/science/article/pii/S2405844020307738NeuroscienceCardiovascular systemCirculatory systemPharmacologyInternal medicineLaboratory medicine |
| spellingShingle | Mei Yang Youcheng Wang Xiaoxing Xiong Baojun Xie Jia Liu Junkui Yin Liuliu Zi Xi Wang Yanhong Tang Congxin Huang Qingyan Zhao SK4 calcium-activated potassium channels activated by sympathetic nerves enhances atrial fibrillation vulnerability in a canine model of acute stroke Heliyon Neuroscience Cardiovascular system Circulatory system Pharmacology Internal medicine Laboratory medicine |
| title | SK4 calcium-activated potassium channels activated by sympathetic nerves enhances atrial fibrillation vulnerability in a canine model of acute stroke |
| title_full | SK4 calcium-activated potassium channels activated by sympathetic nerves enhances atrial fibrillation vulnerability in a canine model of acute stroke |
| title_fullStr | SK4 calcium-activated potassium channels activated by sympathetic nerves enhances atrial fibrillation vulnerability in a canine model of acute stroke |
| title_full_unstemmed | SK4 calcium-activated potassium channels activated by sympathetic nerves enhances atrial fibrillation vulnerability in a canine model of acute stroke |
| title_short | SK4 calcium-activated potassium channels activated by sympathetic nerves enhances atrial fibrillation vulnerability in a canine model of acute stroke |
| title_sort | sk4 calcium activated potassium channels activated by sympathetic nerves enhances atrial fibrillation vulnerability in a canine model of acute stroke |
| topic | Neuroscience Cardiovascular system Circulatory system Pharmacology Internal medicine Laboratory medicine |
| url | http://www.sciencedirect.com/science/article/pii/S2405844020307738 |
| work_keys_str_mv | AT meiyang sk4calciumactivatedpotassiumchannelsactivatedbysympatheticnervesenhancesatrialfibrillationvulnerabilityinacaninemodelofacutestroke AT youchengwang sk4calciumactivatedpotassiumchannelsactivatedbysympatheticnervesenhancesatrialfibrillationvulnerabilityinacaninemodelofacutestroke AT xiaoxingxiong sk4calciumactivatedpotassiumchannelsactivatedbysympatheticnervesenhancesatrialfibrillationvulnerabilityinacaninemodelofacutestroke AT baojunxie sk4calciumactivatedpotassiumchannelsactivatedbysympatheticnervesenhancesatrialfibrillationvulnerabilityinacaninemodelofacutestroke AT jialiu sk4calciumactivatedpotassiumchannelsactivatedbysympatheticnervesenhancesatrialfibrillationvulnerabilityinacaninemodelofacutestroke AT junkuiyin sk4calciumactivatedpotassiumchannelsactivatedbysympatheticnervesenhancesatrialfibrillationvulnerabilityinacaninemodelofacutestroke AT liuliuzi sk4calciumactivatedpotassiumchannelsactivatedbysympatheticnervesenhancesatrialfibrillationvulnerabilityinacaninemodelofacutestroke AT xiwang sk4calciumactivatedpotassiumchannelsactivatedbysympatheticnervesenhancesatrialfibrillationvulnerabilityinacaninemodelofacutestroke AT yanhongtang sk4calciumactivatedpotassiumchannelsactivatedbysympatheticnervesenhancesatrialfibrillationvulnerabilityinacaninemodelofacutestroke AT congxinhuang sk4calciumactivatedpotassiumchannelsactivatedbysympatheticnervesenhancesatrialfibrillationvulnerabilityinacaninemodelofacutestroke AT qingyanzhao sk4calciumactivatedpotassiumchannelsactivatedbysympatheticnervesenhancesatrialfibrillationvulnerabilityinacaninemodelofacutestroke |