{"title":"迷走神经刺激减轻脓毒性休克诱发的大鼠心脏损伤","authors":"Y Chen, M Cui, Y Cui","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>This research aimed to evaluate whether vagus nerve stimulation (VNS) could effectively prevent septic shock-induced cardiac injury in rats and investigate the potential mechanisms. Female Sprague-Dawley rats were divided into the Sham group (sham cecal ligation and puncture [CLP] plus vagal nerve trunk separation), the Vehicle group (CLP plus vagal nerve trunk separation), and the VNS groups (CLP plus vagal nerve trunk separation plus VNS). The left ventricular function was analyzed by echocardiography. Histologic examinations of the cardiac tissues were performed through hematoxylin and eosin staining and TUNEL staining. The Vehicle group had worse cardiac function, higher levels of cardiac injury markers, and enhanced myocardial apoptosis than the Sham group. The rats in the VNS groups had enhanced cardiac function, lower levels of cardiac injury markers, and inhibited myocardial apoptosis than those in the Vehicle group. Elevated interleukin-1beta and tumor necrosis factor-alpha-levels and activated nuclear factor kappa B (NF-kappa-B) signal in septic shock rats were inhibited by the performance of VNS. This study suggests that VNS contributes to the reduction of myocardial apoptosis and improvement of left ventricular function to attenuate septic shock-induced cardiac injury in rats. The performance of VNS inhibits the inflammatory responses in heart tissues via the regulation of NF-kappa-B signal.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":null,"pages":null},"PeriodicalIF":1.9000,"publicationDate":"2023-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10805250/pdf/","citationCount":"0","resultStr":"{\"title\":\"Vagus nerve stimulation attenuates septic shock-induced cardiac injury in rats.\",\"authors\":\"Y Chen, M Cui, Y Cui\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>This research aimed to evaluate whether vagus nerve stimulation (VNS) could effectively prevent septic shock-induced cardiac injury in rats and investigate the potential mechanisms. Female Sprague-Dawley rats were divided into the Sham group (sham cecal ligation and puncture [CLP] plus vagal nerve trunk separation), the Vehicle group (CLP plus vagal nerve trunk separation), and the VNS groups (CLP plus vagal nerve trunk separation plus VNS). The left ventricular function was analyzed by echocardiography. Histologic examinations of the cardiac tissues were performed through hematoxylin and eosin staining and TUNEL staining. The Vehicle group had worse cardiac function, higher levels of cardiac injury markers, and enhanced myocardial apoptosis than the Sham group. The rats in the VNS groups had enhanced cardiac function, lower levels of cardiac injury markers, and inhibited myocardial apoptosis than those in the Vehicle group. Elevated interleukin-1beta and tumor necrosis factor-alpha-levels and activated nuclear factor kappa B (NF-kappa-B) signal in septic shock rats were inhibited by the performance of VNS. This study suggests that VNS contributes to the reduction of myocardial apoptosis and improvement of left ventricular function to attenuate septic shock-induced cardiac injury in rats. The performance of VNS inhibits the inflammatory responses in heart tissues via the regulation of NF-kappa-B signal.</p>\",\"PeriodicalId\":20235,\"journal\":{\"name\":\"Physiological research\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.9000,\"publicationDate\":\"2023-12-31\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10805250/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Physiological research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"PHYSIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Physiological research","FirstCategoryId":"3","ListUrlMain":"","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
Vagus nerve stimulation attenuates septic shock-induced cardiac injury in rats.
This research aimed to evaluate whether vagus nerve stimulation (VNS) could effectively prevent septic shock-induced cardiac injury in rats and investigate the potential mechanisms. Female Sprague-Dawley rats were divided into the Sham group (sham cecal ligation and puncture [CLP] plus vagal nerve trunk separation), the Vehicle group (CLP plus vagal nerve trunk separation), and the VNS groups (CLP plus vagal nerve trunk separation plus VNS). The left ventricular function was analyzed by echocardiography. Histologic examinations of the cardiac tissues were performed through hematoxylin and eosin staining and TUNEL staining. The Vehicle group had worse cardiac function, higher levels of cardiac injury markers, and enhanced myocardial apoptosis than the Sham group. The rats in the VNS groups had enhanced cardiac function, lower levels of cardiac injury markers, and inhibited myocardial apoptosis than those in the Vehicle group. Elevated interleukin-1beta and tumor necrosis factor-alpha-levels and activated nuclear factor kappa B (NF-kappa-B) signal in septic shock rats were inhibited by the performance of VNS. This study suggests that VNS contributes to the reduction of myocardial apoptosis and improvement of left ventricular function to attenuate septic shock-induced cardiac injury in rats. The performance of VNS inhibits the inflammatory responses in heart tissues via the regulation of NF-kappa-B signal.
期刊介绍:
Physiological Research is a peer reviewed Open Access journal that publishes articles on normal and pathological physiology, biochemistry, biophysics, and pharmacology.
Authors can submit original, previously unpublished research articles, review articles, rapid or short communications.
Instructions for Authors - Respect the instructions carefully when submitting your manuscript. Submitted manuscripts or revised manuscripts that do not follow these Instructions will not be included into the peer-review process.
The articles are available in full versions as pdf files beginning with volume 40, 1991.
The journal publishes the online Ahead of Print /Pre-Press version of the articles that are searchable in Medline and can be cited.