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

Min Yang,Zhengfei Yang,Jun Li,Yangyang Zou,Xiaohui Huang,Tianfeng Hua,Limin Chen

doi:10.1155/2020/6969053

Abstract

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, 3 min; maintenance dose: 0.01 α (TNF-α (TNF-α (TNF-κB (NF-κB (NF-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 (TNF-κB (NF-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.α (TNF-κB (NF-

Highlights

Cardiopulmonary resuscitation (CPR) improves the restoration of spontaneous circulation (ROSC) rate in cardiac arrest (CA) patients. e survival rate following CA remains unsatisfactory, and the survival-to-discharge ratios following out-of-hospital and in-hospital adult CA episodes are 7.9% and 21%, respectively, in the USA [1]. e severity of postresuscitation syndrome (PRS) is closely related to both the survival rates and the long-term outcomes of CA patients, with more than 70% of patients dying within 72 h after ROSC [2, 3]
Heart tissues were evaluated by light microscopy. e protein expression levels of myocardial inflammatory factors (IL6 and tumor necrosis factor-α (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. e administration of Recombinant human brain natriuretic peptide (rhBNP) attenuated the severity of postresuscitation myocardial dysfunction (PRMD) and myocardial tissue injuries, with improvement of mean aortic pressure (MAP), End-tidal CO2 (ETCO2), serum level of NT-proBNP, ejection fraction (EF), cardiac output (CO), and myocardial performance index (MPI) values. e 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

Summary

Research Article

The time of cardiopulmonary resuscitation was 8 min, after which defibrillation was attempted in this rat model. E 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. E 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. 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 reduced the serum and myocardial tissue levels of IL-6 and TNF-α after ROSC, likely due to the suppression of the TLR4/NFκB signaling pathway and the regulation of inflammatory mediator secretion 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 reduced the serum and myocardial tissue levels of IL-6 and TNF-α after ROSC, likely due to the suppression of the TLR4/NFκB signaling pathway and the regulation of inflammatory mediator secretion

Introduction

Materials and Methods

Results

Group con rhBNP