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Updated: Jun 24, 2026

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing
Published on: December 11, 2017
[Effects of neregulin on rhesus monkey heart failure induced by rapid pacing]
Xiao-Bo Liu1, Jiang Li, Yi Xiao
1National Chengdu Center for Safety Evaluation of Traditional Chinese Medicine, West China Hospital, Sichuan University, Chengdu 610041, China.
Objective:
To investigate the effects of Recombined Human Neuregulin (NRG) on the expression of Glucose transporter (Glut1) in myocardium tissue of Rhesus Monkeys with Pacing-induced Heart Failure and the heart function.
Methods:
Twenty four rhesus monkeys were randomly divided into three groups (shame operated group, heart failure group and NRG treated group), each with 8 monkeys. Heart failures were induced by rapid pacing (240 heart beats/min). Daily intravenous injection of recombined human NRG [3 microg/(kg x d)] and normal saline were given to the monkeys for 10 days for the NRG treated group and heart failure group respectively. Hemodynamic measurements including +dp/dt(max) and left ventricular systolic, end-diastolic blood pressures (LVSP and LVEDP) were conducted. The RT-PCR was applied to detect the expression level of PKB, Glut1 mRNA in the left ventricular cardiac muscle.
Results:
The monkeys in the heart failure group had lower levels of + dp/dt(max) and LVSP and higher levels of LVEDP than those in the shame operated group (P < 0.05). The monkeys in the NRG treated group had higher levels of +dp/dt(max) than those in the heart failure group (P < 0.05). Lower expression of PKB, Glut1 mRNA in the heart failure group was observed compared with the shame operated group (P < 0.05) while the NRG treated group had a higher expression level of PKB,Glut1 mRNA by compared with the heart failure group (P < 0.05).
Conclusion:
Recombined human NRG can relieve heart failure syndroms through up-regulating the expression of PKB, Glut1 mRNA and improving energy supply of the ischemic cardiac muscle.

