Abstract 3681: Ultrasound Triggered Nitric Oxide Release from Echogenic Liposomes Improves Arterial Vasodilation
Background: Nitric oxide (NO) has been identified as a vasodilator. Delivering external NO to the arterial wall is hampered by hemoglobin scavenging. NO-containing echogenic liposomes (EL) can protect NO from hemoglobin scavenging. We hypothesize that ultrasound can further enhance and control NO release from the NO-EL with resultant arterial vasodilation.
Methods: NO-EL composed of phospholipids and cholesterol were prepared by a pressurization-freeze method. Rabbit carotid arteries were collected and placed in to an open flow system. Doppler ultrasound (fc=5.7 MHz, MI=0.15, PRF=8 kHz) was utilized to trigger NO release for 30 seconds upon NO-EL administration using a linear transvascular ultrasound transducer (Vivid.i, GE Health Care). To determine vasodilation, diameters of arterial sections were measured with ultrasound as well as microscopy at baseline and 3 minutes after NO-EL administration under control and Doppler ultrasound treatment. Each artery was washed and snap-frozen for fluorescent microscopy (DAF-2 DA).
Results: Both NO only (4.8±2.11%) and NO-Doppler ultrasound (9.8±2.23%) demonstrated vasodilation compared to baseline (p<0.05). Doppler ultrasound further enhanced NO release from NO-EL with greater arterial enlargement (p<0.05). Histology confirmed greater NO infiltration into the arterial wall in the Doppler ultrasound treatment group. NO induced vasodilation from the NO-EL lasted for up to 5 minutes.
Conclusion: Doppler ultrasound can trigger NO release from NO-EL facilitating NO delivery and effect into the arterial wall. This NO delivery strategy may improve targeted therapeutic delivery into vascular tissues.