Electroporation-induced changes in normal immature rat myoblasts (H9C2)

Area of Science:

• Biomedical Engineering
• Cardiovascular Research
• Cell Biology

Background:

• High electric fields are used in defibrillation but can cause irreversible electroporation (EP) and tissue damage.
• Electroporation (EP) can lead to cell destruction if transmembrane potentials are sufficiently high.
• Adverse cardiac effects from electroporation (EP) are a concern, especially with nearby electrochemotherapy.

Purpose of the Study:

• To investigate the effects of electroporation (EP) on cardiac cell cultures (H9C2).
• To determine the threshold electric field intensity for cell membrane disruption and cell death in cardiomyocytes.
• To assess apoptosis and necrosis following electroporation (EP) in cardiac cells.

Main Methods:

• Cardiac H9C2 cells were exposed to short electric field pulses (25-3250 V/cm, 50 µs).
• Cell viability was assessed using MTT assay 24 hours post-electroporation (EP).
• DNA fragmentation (apoptosis) was analyzed via alkaline and neutral comet assays; cell morphology was observed via phase contrast microscopy.

Main Results:

• High-intensity electroporation (EP) disrupted cell membranes, visible in phase contrast images.
• Comet assays showed minimal apoptosis (few percent) and no necrosis 2 hours post-electroporation (EP).
• MTT viability assays indicated that electric field intensities above 375 V/cm were destructive to cardiomyocyte viability.

Conclusions:

• Electroporation (EP) at intensities below 375 V/cm causes transient membrane disruption but limited apoptosis in H9C2 cells.
• Higher electric field intensities (>375 V/cm) are required to induce significant cell death in cardiac cells via electroporation (EP).
• These findings are crucial for understanding the safety limits of electroporation (EP) in cardiac applications and minimizing adverse effects.