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Electrophysiology of papillary muscle in SAH: changes and N-acetylcysteine protection
Murat Ayaz1, Onder Guney, Fatih Erdi
1Selçuk University, Meram Medical Faculty, Department of Biophysics, 42080, Meram, Konya, Turkey. ayaz72@yahoo.com
Insights
Subarachnoid hemorrhage (SAH) causes cardiac dysfunction by altering ventricular action potentials and contraction. N-acetylcysteine (NAC) pretreatment effectively protected cardiac function in this model.
Area of Science:
- Cardiology
- Neurology
- Pharmacology
Background:
- Subarachnoid hemorrhage (SAH) is a model for studying heart-brain interactions.
- Cardiac changes following SAH, including effects on single ventricular action potential (SVAP) and contraction, remain understudied.
- The cardioprotective potential of agents like N-acetylcysteine (NAC) in SAH has not been investigated.
Purpose of the Study:
- To investigate the impact of SAH on SVAP and cardiac contraction in rabbits.
- To evaluate the cardioprotective effects of N-acetylcysteine (NAC) in SAH.
Main Methods:
- SAH was induced in male rabbits by replacing cerebrospinal fluid with autologous blood.
- A control group received serum physiologic, while the SAH group was treated with N-acetylcysteine (NAC) daily for 3 days.
- Single ventricular action potential and left ventricular papillary muscle contraction were recorded.
Main Results:
- SAH led to decreased action potential overshoot, prolonged repolarization, and depressed resting membrane potential.
- Cardiac muscle exhibited reduced peak tension and increased time to peak contraction after SAH.
- NAC treatment prevented these SAH-induced pathological cardiac changes.
Conclusions:
- SAH induces cardiac dysfunction, potentially via mitochondrial dysfunction and ATP depletion.
- N-acetylcysteine (NAC) pretreatment demonstrated a protective effect against SAH-induced cardiac alterations.
- Further research is needed to elucidate the precise mechanism of NAC's cardioprotective action in SAH.
Background:
Although subarachnoid hemorrhage (SAH) serves as a good model to study heart-brain interactions, neither the changes on the single ventricular action potential (SVAP) and contraction nor the effects of possible cardioprotective agents have been investigated.
Materials And Methods:
A total of 18 male rabbits were used for the three experimental groups. SAH was induced by replacing the cerebrospinal fluid (CSF) with fresh autologous blood at the ratio of 1 mL to the 1-kg body mass (N = 6). In the control (CON; N = 6) group, the CSF was replaced with serum physiologic at the same ratio. The treated SAH group (SAH+NAC) received daily intraperitoneal N-acetylcysteine (NAC; 150 mg/kg for 3 days) starting from just before SAH was induced by CSF replacement. On the fourth day, animals were examined for the single action potential and contraction recordings from the left ventricular papillary muscle.
Results:
At the end of 3 days, the overshoot decreased together with increased time to reach the peak potential. Additionally, the resting membrane potential was depressed and repolarization was slowed during SVAPs. On the other hand, peak tension depressed and time to peak increased. NAC treatment, which protects infarction in the brain, prevented these pathological changes in the cardiac muscle.
Conclusion:
SAH-induced cardiac changes can be attributed to adenosine triphosphate depletion through mitochondrial dysfunction. Pretreatment of NAC to SAH on the other hand had a positive effect on these cardiac changes. But the exact mechanism by which NAC treatment protects the cardiac muscle needs further investigation.
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