Left-sided vagus nerve stimulation improves cardiopulmonary resuscitation outcomes in rats as effectively as right-sided vagus nerve stimulation.
Cardiac arrest
Myocardial function
Tumor necrosis factor-alpha
Vagus nerve stimulation
α-7 nicotinic acetylcholine receptor
Journal
World journal of emergency medicine
ISSN: 1920-8642
Titre abrégé: World J Emerg Med
Pays: China
ID NLM: 101549691
Informations de publication
Date de publication:
2021
2021
Historique:
received:
12
01
2021
accepted:
22
06
2021
entrez:
13
9
2021
pubmed:
14
9
2021
medline:
14
9
2021
Statut:
ppublish
Résumé
Our group previously reported that right-sided vagus nerve stimulation (RVNS) significantly improved outcomes after cardiopulmonary resuscitation (CPR) in a rat model of cardiac arrest (CA). However, whether left-sided vagus nerve stimulation (LVNS) could achieve the same effect as RVNS in CPR outcomes remains unknown. A rat model of CA was established using modified percutaneous epicardial electrical stimulation to induce ventricular fibrillation (VF). Rats were treated with LVNS or RVNS for 30 minutes before the induction of VF. All animals were observed closely within 72 hours after return of spontaneous circulation (ROSC), and their health and behavior were evaluated every 24 hours. Compared with those in the RVNS group, the hemodynamic measurements in the LVNS group decreased more notably. Vagus nerve stimulation (VNS) decreased the serum levels of tumor necrosis factor-alpha (TNF-α) and the arrhythmia score, and attenuated inflammatory infiltration in myocardial tissue after ROSC, regardless of the side of stimulation, compared with findings in the CPR group. Both LVNS and RVNS ameliorated myocardial function and increased the expression of α-7 nicotinic acetylcholine receptor in the myocardium after ROSC. Moreover, a clear improvement in 72-hour survival was shown with VNS pre-treatment, with no significant difference in efficacy when comparing the laterality of stimulation. LVNS may have similar effects as RVNS on improving outcomes after CPR.
Sections du résumé
BACKGROUND
BACKGROUND
Our group previously reported that right-sided vagus nerve stimulation (RVNS) significantly improved outcomes after cardiopulmonary resuscitation (CPR) in a rat model of cardiac arrest (CA). However, whether left-sided vagus nerve stimulation (LVNS) could achieve the same effect as RVNS in CPR outcomes remains unknown.
METHODS
METHODS
A rat model of CA was established using modified percutaneous epicardial electrical stimulation to induce ventricular fibrillation (VF). Rats were treated with LVNS or RVNS for 30 minutes before the induction of VF. All animals were observed closely within 72 hours after return of spontaneous circulation (ROSC), and their health and behavior were evaluated every 24 hours.
RESULTS
RESULTS
Compared with those in the RVNS group, the hemodynamic measurements in the LVNS group decreased more notably. Vagus nerve stimulation (VNS) decreased the serum levels of tumor necrosis factor-alpha (TNF-α) and the arrhythmia score, and attenuated inflammatory infiltration in myocardial tissue after ROSC, regardless of the side of stimulation, compared with findings in the CPR group. Both LVNS and RVNS ameliorated myocardial function and increased the expression of α-7 nicotinic acetylcholine receptor in the myocardium after ROSC. Moreover, a clear improvement in 72-hour survival was shown with VNS pre-treatment, with no significant difference in efficacy when comparing the laterality of stimulation.
CONCLUSIONS
CONCLUSIONS
LVNS may have similar effects as RVNS on improving outcomes after CPR.
Identifiants
pubmed: 34512829
doi: 10.5847/wjem.j.1920-8642.2021.04.010
pii: WJEM-12-309
pmc: PMC8390357
doi:
Types de publication
Journal Article
Langues
eng
Pagination
309-316Informations de copyright
Copyright: © World Journal of Emergency Medicine.
Déclaration de conflit d'intérêts
Conflicts of interests: The authors declare that they have no competing interests.
Références
Med Sci Monit. 2017 Dec 23;23:6072-6081
pubmed: 29274273
Cardiovasc Res. 1988 Jul;22(7):447-55
pubmed: 3252968
J Intensive Care Med. 2020 Mar;35(3):219-224
pubmed: 30526209
Am J Physiol. 1993 Aug;265(2 Pt 2):H681-90
pubmed: 8368370
Annu Int Conf IEEE Eng Med Biol Soc. 2018 Jul;2018:3681-3684
pubmed: 30441171
Am J Physiol Heart Circ Physiol. 2015 Nov 15;309(10):H1740-52
pubmed: 26371171
Exp Physiol. 2017 Mar 1;102(3):385
pubmed: 28247476
Crit Care Med. 2004 Aug;32(8):1753-8
pubmed: 15286554
J Neurosurg Anesthesiol. 2008 Jan;20(1):29-35
pubmed: 18157022
Am J Physiol Heart Circ Physiol. 2014 Sep 1;307(5):H722-31
pubmed: 25015962
Int J Cardiol. 2017 Jan 15;227:704-710
pubmed: 27816306
Nature. 2003 Jan 23;421(6921):384-8
pubmed: 12508119
Shock. 2018 Jun;49(6):698-703
pubmed: 28800036
Int J Cardiol. 2014 Oct 20;176(3):1030-2
pubmed: 25156835
Physiol Rep. 2017 Apr;5(7):
pubmed: 28400500
Heart Rhythm. 2013 Nov;10(11):1700-7
pubmed: 23933295
Clin Exp Pharmacol Physiol. 2010 Dec;37(12):1114-9
pubmed: 20880185
J Cardiovasc Electrophysiol. 2008 Mar;19(3):309-15
pubmed: 18070031
Exp Physiol. 2014 Feb;99(2):295-9
pubmed: 24014808
J Neurochem. 2015 Jul;134(1):173-81
pubmed: 25783636
Circulation. 2002 Jul 30;106(5):562-8
pubmed: 12147537
J Card Fail. 2014 Nov;20(11):808-16
pubmed: 25187002