Related Experiment Video
Updated: Sep 27, 2026

Isolation of Human Ventricular Cardiomyocytes from Vibratome-Cut Myocardial Slices
Published on: May 10, 2020
Magnesium reduces free radical concentration and preserves left ventricular function after direct current shocks
Yi Zhang1, Loyd R Davies, Sean M Martin
1Department of Internal Medicine, The Cardiovascular Center, College of Medicine, University of Iowa Hospital, 200 Hawkins Drive, Iowa City, IA 52242, USA.
Objective:
Our objective was to determine if magnesium reduces free radicals generated by direct current countershock and preserves left ventricular contractile function.
Background:
We have previously shown that magnesium reduces free radicals in a coronary occlusion-reperfusion model, and therefore also might reduce free radical generation by direct current shocks.
Methods:
In eight swine weighing 18-27 kg (mean: 22 kg), using electron paramagnetic resonance, we monitored continuously the coronary sinus concentration of ascorbate free radical, a measure of free radical generation (total oxidative flux). Epicardial shocks (30 J) using a truncated exponential biphasic waveform (5/5 ms) were administered. Each animal received two shocks, one without and one with magnesium, 80 mg/min IV, beginning 10 min before the shock and continuing to 15 min after the shock. Percent fractional area shortening of the left ventricular cavity was determined by 2-dimensional echocardiography.
Results:
Magnesium shocks resulted in a significantly lower increase in the ascorbate free radical concentration (0.6+/-4.6%) than no-magnesium shocks (16+/-3.3%, P<0.05) at 12 min after the shock. Total radical flux was reduced 72% (P<0.05), and left ventricular fractional area shortening was preserved: baseline: 69+/-2.6%, no-magnesium shocks: 41+/-2.8% (P<0.05, versus baseline) and magnesium shocks 61+/-3.7%.
Conclusions:
Magnesium pre-treatment reduced oxygen free radicals generated by direct current shocks; post-shock left ventricular contractile function was not impaired. Magnesium may be cardioprotective during epicardial ('surgical') defibrillation.
Insights
Magnesium pre-treatment significantly reduced oxygen free radicals from direct current shocks. This intervention preserved left ventricular function, suggesting magnesium may offer cardioprotection during defibrillation.
Area of Science:
- Cardiology
- Biochemistry
- Medical Devices
Background:
- Previous research indicated magnesium's ability to mitigate free radicals in a coronary occlusion-reperfusion model.
- This study investigated magnesium's potential to reduce free radical generation specifically from direct current (DC) shocks.
Purpose of the Study:
- To ascertain if magnesium administration can decrease free radicals produced by DC countershock.
- To evaluate the impact of magnesium on preserving left ventricular contractile function following DC shock.
Main Methods:
- Eight swine underwent electron paramagnetic resonance to monitor coronary sinus ascorbate free radical concentration, a marker for total oxidative flux.
- Epicardial shocks (30 J, biphasic waveform) were delivered with and without magnesium (80 mg/min IV).
- Left ventricular fractional area shortening was assessed via 2-dimensional echocardiography to measure contractile function.
Main Results:
- Magnesium administration significantly reduced the post-shock increase in ascorbate free radical concentration (0.6% vs. 16%, P<0.05).
- Total radical flux was decreased by 72% (P<0.05) with magnesium treatment.
- Left ventricular fractional area shortening was preserved with magnesium (61%) compared to no-magnesium shocks (41%, P<0.05 vs. baseline).
Conclusions:
- Magnesium pre-treatment effectively reduced oxygen free radicals generated by DC shocks.
- Post-shock left ventricular contractile function remained unimpaired in the presence of magnesium.
- Magnesium demonstrates potential cardioprotective effects during epicardial (surgical) defibrillation.
Related Concept Videos
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Myocarditis III: Medical Management
Heart Failure Drugs: Inotropic Agents

