Abstract 109: Nitric Oxide Added to the ECMO Circuit Improves Neuroprotection and Cardiac Function After Cardiac Arrest

Background: Veno-arterial extracorporeal life support (ECLS) is increasingly used in patients during cardiac arrest. Nitric Oxide (NO) has shown potential for exerting a protective role in ischemia/reperfusion damage in different organs.

Aim: This study aims to investigate the cardio and neuroprotective effects of NO administered in the extracorporeal membrane oxygenation (ECMO) circuit after cardiac arrest.

Methods: Thirty male SD rats were subjected to 10 minutes of cardiac arrest. They were randomly assigned to receive ECMO or ECMO plus NO (20 ppm) administered in the oxygenator (ECMO+NO). After 1 hour, the animals were weaned from ECMO, hemodynamic analysis using pressure-volume miniaturized catheter, and cardiac and brain samples were collected after two hours.

Results: Analysis of cardiac function showed improved systolic cardiac function in the ECMO+NO group compared to standard ECMO (stroke volume: 55 ± 8 vs. 26 ± 9 μl, cardiac index: 9.05 ± 1.41 vs. 4.70 ± 0.81 ml/min/100g, dP/dt _max : 6870 ± 290 vs. 5124 ± 205 mmHg/s; p<0.01). The ECMO+NO group also exhibited reduced systemic resistance (total peripheral resistance: 2.14 ± 0.42 vs. 2.95 ± 0.35 mmHg/ml/min/100g; p<0.05) and improved ventricular-arterial coupling (Ees/Ea: 0.96 ± 0.15 vs. 0.53 ± 0.15; p<0.001). Neuroinflammation, assessed by the expression of Iba1, a microglia activation marker, was attenuated in the ECMO+NO group (8.37 ± 0.41% vs. 12.58 ± 0.48%; p < 0.001). The extent of hypoxic brain areas, analyzed by thiol oxidation, was lower in the ECMO+NO group (4.07 ± 0.45% vs. 11.72 ± 1.03%; p<0.01).

Conclusions: NO administration in the oxygenator during ECMO after cardiac arrest improves cardiac function and ventricular-arterial coupling and enhances neuroprotection decreasing neuroinflammation and hypoxic areas. NO administration in the ECMO circuit might be a promising therapeutic adjunct during ECLS.