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Updated: Dec 26, 2025
A Rat Model of Ventricular Fibrillation and Resuscitation by Conventional Closed-chest Technique
Published on: April 26, 2015
The Protective Effect of rhBNP on Postresuscitation Myocardial Dysfunction in a Rat Cardiac Arrest Model
Min Yang1,2,3, Tianfeng Hua2,3, Zhengfei Yang3
1Department of Basic and Clinical Pharmacology, School of Pharmacy, Anhui Medical University, Hefei, China.
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.
