The Protective Effect of rhBNP on Postresuscitation Myocardial Dysfunction in a Rat Cardiac Arrest Model

Purpose. We investigated the protective effects and the underlying mechanisms through which recombinant human brain natriuretic peptide (rhBNP) acts on postresuscitation myocardial dysfunction (PRMD) in the cardiac arrest (CA) model. Methods. Ventricular fibrillation was induced and untreated for 6 ...

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Main Authors: Min Yang, Tianfeng Hua, Zhengfei Yang, Limin Chen, Yangyang Zou, Xiaohui Huang, Jun Li
Format: Article
Language:English
Published: Hindawi Limited 2020-01-01
Series:BioMed Research International
Online Access:http://dx.doi.org/10.1155/2020/6969053
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spelling doaj-05db0a68cd0142019d7d685ac1370cd42020-11-25T02:21:17ZengHindawi LimitedBioMed Research International2314-61332314-61412020-01-01202010.1155/2020/69690536969053The Protective Effect of rhBNP on Postresuscitation Myocardial Dysfunction in a Rat Cardiac Arrest ModelMin Yang0Tianfeng Hua1Zhengfei Yang2Limin Chen3Yangyang Zou4Xiaohui Huang5Jun Li6Department of Basic and Clinical Pharmacology, School of Pharmacy, Anhui Medical University, Hefei, ChinaDepartment of Intensive Care Unit, The Second Affiliated Hospital of Anhui Medical University, Hefei, ChinaInstitute of Cardiopulmonary Cerebral Resuscitation, Sun Yat-sen University, Guangzhou, ChinaDepartment of Intensive Care Unit, The Second Affiliated Hospital of Anhui Medical University, Hefei, ChinaDepartment of Intensive Care Unit, The Second Affiliated Hospital of Anhui Medical University, Hefei, ChinaDepartment of Basic and Clinical Pharmacology, School of Pharmacy, Anhui Medical University, Hefei, ChinaDepartment of Basic and Clinical Pharmacology, School of Pharmacy, Anhui Medical University, Hefei, ChinaPurpose. We investigated the protective effects and the underlying mechanisms through which recombinant human brain natriuretic peptide (rhBNP) acts on postresuscitation myocardial dysfunction (PRMD) in the cardiac arrest (CA) model. Methods. Ventricular fibrillation was induced and untreated for 6 min. And the time of cardiopulmonary resuscitation was 8 min, after which defibrillation was attempted in this rat model. 24 Sprague Dawley rats (450–550g) were randomized into cardiopulmonary resuscitation (CPR) + rhBNP and CPR + placebo groups after restoration of spontaneous circulation (ROSC). rhBNP was infused at PR 30 min (loading dose: 1.5 µg/kg, 3 min; maintenance dose: 0.01 µg/kg/min, 6 h). Vital signs, ejection fraction (EF), cardiac output (CO), myocardial performance index (MPI), and 24 h survival rate were continuously recorded. The serum levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and N-terminal probrain natriuretic peptide (NT-proBNP) were detected by ELISA. Heart tissues were evaluated by light microscopy. The protein expression levels of myocardial inflammatory factors (IL-6 and TNF-α), Toll-like receptor 4 (TLR4), nuclear transcription factor-κB (NF-κB) subunit p65 (p65), and phosphor-p65 were analyzed by western blotting. Results. The administration of rhBNP attenuated the severity of PRMD and myocardial tissue injuries, with improvement of MAP (mean arterial blood pressure), ETCO2 (end-tidal CO2), serum level of NT-proBNP, EF, CO, and MPI values. The serum levels and protein expression levels in myocardial tissue of IL-6 and TNF-α after ROSC were reduced by inhibiting the expression of TLR4/NF-κB. Conclusion. Our research demonstrated that the administration of rhBNP attenuated the severity of PRMD and myocardial tissue injuries and increased the 24 h survival rate in this CA model. rhBNP administration also reduced the serum and myocardial tissue levels of IL-6 and TNF-α after ROSC, likely due to the suppression of the TLR4/NF-κB signaling pathway and the regulation of inflammatory mediator secretion.http://dx.doi.org/10.1155/2020/6969053
collection DOAJ
language English
format Article
sources DOAJ
author Min Yang
Tianfeng Hua
Zhengfei Yang
Limin Chen
Yangyang Zou
Xiaohui Huang
Jun Li
spellingShingle Min Yang
Tianfeng Hua
Zhengfei Yang
Limin Chen
Yangyang Zou
Xiaohui Huang
Jun Li
The Protective Effect of rhBNP on Postresuscitation Myocardial Dysfunction in a Rat Cardiac Arrest Model
BioMed Research International
author_facet Min Yang
Tianfeng Hua
Zhengfei Yang
Limin Chen
Yangyang Zou
Xiaohui Huang
Jun Li
author_sort Min Yang
title The Protective Effect of rhBNP on Postresuscitation Myocardial Dysfunction in a Rat Cardiac Arrest Model
title_short The Protective Effect of rhBNP on Postresuscitation Myocardial Dysfunction in a Rat Cardiac Arrest Model
title_full The Protective Effect of rhBNP on Postresuscitation Myocardial Dysfunction in a Rat Cardiac Arrest Model
title_fullStr The Protective Effect of rhBNP on Postresuscitation Myocardial Dysfunction in a Rat Cardiac Arrest Model
title_full_unstemmed The Protective Effect of rhBNP on Postresuscitation Myocardial Dysfunction in a Rat Cardiac Arrest Model
title_sort protective effect of rhbnp on postresuscitation myocardial dysfunction in a rat cardiac arrest model
publisher Hindawi Limited
series BioMed Research International
issn 2314-6133
2314-6141
publishDate 2020-01-01
description Purpose. We investigated the protective effects and the underlying mechanisms through which recombinant human brain natriuretic peptide (rhBNP) acts on postresuscitation myocardial dysfunction (PRMD) in the cardiac arrest (CA) model. Methods. Ventricular fibrillation was induced and untreated for 6 min. And the time of cardiopulmonary resuscitation was 8 min, after which defibrillation was attempted in this rat model. 24 Sprague Dawley rats (450–550g) were randomized into cardiopulmonary resuscitation (CPR) + rhBNP and CPR + placebo groups after restoration of spontaneous circulation (ROSC). rhBNP was infused at PR 30 min (loading dose: 1.5 µg/kg, 3 min; maintenance dose: 0.01 µg/kg/min, 6 h). Vital signs, ejection fraction (EF), cardiac output (CO), myocardial performance index (MPI), and 24 h survival rate were continuously recorded. The serum levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and N-terminal probrain natriuretic peptide (NT-proBNP) were detected by ELISA. Heart tissues were evaluated by light microscopy. The protein expression levels of myocardial inflammatory factors (IL-6 and TNF-α), Toll-like receptor 4 (TLR4), nuclear transcription factor-κB (NF-κB) subunit p65 (p65), and phosphor-p65 were analyzed by western blotting. Results. The administration of rhBNP attenuated the severity of PRMD and myocardial tissue injuries, with improvement of MAP (mean arterial blood pressure), ETCO2 (end-tidal CO2), serum level of NT-proBNP, EF, CO, and MPI values. The serum levels and protein expression levels in myocardial tissue of IL-6 and TNF-α after ROSC were reduced by inhibiting the expression of TLR4/NF-κB. Conclusion. Our research demonstrated that the administration of rhBNP attenuated the severity of PRMD and myocardial tissue injuries and increased the 24 h survival rate in this CA model. rhBNP administration also reduced the serum and myocardial tissue levels of IL-6 and TNF-α after ROSC, likely due to the suppression of the TLR4/NF-κB signaling pathway and the regulation of inflammatory mediator secretion.
url http://dx.doi.org/10.1155/2020/6969053
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