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Updated: Jul 26, 2025
Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
Published on: June 18, 2021
Transient cardiac electrophysiological changes in a rat model of subarachnoid haemorrhage: a brain-heart interaction
Mingxian Chen1, Zhuo Wang2, Xin Lai2
1Department of Cardiology, The Second Xiangya Hospital of Central South University, Renmin Road, Furong District, Changsha 410011, China.
Insights
Subarachnoid hemorrhage (SAH) increases sudden cardiac death risk by causing temporary ventricular arrhythmias. This is linked to heightened sympathetic activity and neuropeptide Y 1 receptor (NPY1R) expression in the acute phase.
Area of Science:
- Cardiology
- Neuroscience
- Physiology
Background:
- Subarachnoid hemorrhage (SAH) is a known cause of sudden cardiac death (SCD).
- The electrophysiological changes and underlying mechanisms of ventricular arrhythmias (VAs) following SAH are not fully understood.
- Understanding these effects is crucial for managing SAH patients and preventing cardiac events.
Purpose of the Study:
- To investigate the long-term effects of SAH on ventricular electrophysiology.
- To explore the potential mechanisms, including sympathetic activity and neuropeptide Y signaling, contributing to VAs after SAH.
Main Methods:
- Utilized a rat model of SAH, assessing electrophysiological parameters (QTc interval, ERP, VFT) and left stellate ganglion (LSG) activity at multiple time points.
- Measured plasma and myocardial neuropeptide Y (NPY) levels and NPY 1 receptor (NPY1R) expression (protein and mRNA).
Main Results:
- SAH induced transient electrophysiological changes, including prolonged QTc, shortened ERP, and reduced VFT, peaking on Day 3.
- Increased LSG activity, NPY levels, and NPY1R expression were observed in the acute phase, also peaking on Day 3.
- These changes normalized by Day 14, indicating a transient susceptibility to VAs.
Conclusions:
- SAH transiently increases susceptibility to ventricular arrhythmias in the acute phase.
- Increased sympathetic activity and upregulated NPY1R expression are key mechanisms driving these arrhythmias post-SAH.
Aims:
Subarachnoid haemorrhage (SAH) is one of the causes of sudden cardiac death (SCD). However, the time course of ventricular arrhythmias and potential mechanisms responsible for this effect after SAH remain unknown.
Objective:
This study aims to investigate the effect of SAH on ventricular electrophysiological changes and its potential mechanisms in long-term phase.
Methods And Results:
We examined the ventricular electrophysiological remodelling and potential mechanisms in a Sprague Dawley rat model of SAH at six time points (baseline, and Days 1, 3, 7, 14 and 28) and explored the potential mechanisms. We measured the ventricular effective refractory period (ERP), ventricular fibrillation threshold (VFT) and left stellate ganglion (LSG) activity at different time points before and after SAH. We also detected neuropeptide Y (NPY) levels in plasma and myocardial tissues by enzyme-linked immunosorbent assay, and quantified NPY 1 receptor (NPY1R) protein and mRNA expression levels by western blotting and quantitative real-time reverse transcription-polymerase chain reaction, respectively. Subarachnoid haemorrhage gradually prolonged QTc intervals, shortened ventricular ERP and reduced VFT during the acute phase, peaking at Day 3. However, no significant changes were observed from Days 14 to 28 compared to Day 0. Subarachnoid haemorrhage gradually increased LSG activity, increased NPY concentrations and up-regulated NPY1R expression in the acute phase of SAH, peaking at Day 3. However, no significant variations were found from Days 14 to 28 compared to Day 0.
Conclusion:
Subarachnoid haemorrhage increases the transient susceptibility of VAs in the acute phase, and the underlying mechanisms for this response included increased sympathetic activity and up-regulated NPY1R expression.
