Nanosecond Pulse Electric Field Activation of Platelet-Rich Plasma Reduces Myocardial Infarct Size and Improves Left Ventricular Mechanical Function in the Rabbit Heart

In the current study, we used the novel, nonchemical method of nanosecond pulsed electric fields (nsPEF) to investigate the efficiency of a protocol involving the in vivo treatment of the ischemic and reperfused heart and heart cells in culture with platelet-rich plasma
(PRP). Associated with the restoration of blood flow to the ischemic
tissue is a phenomenon referred to as “ischemic reperfusion injury.”
Clinically a type of reperfusion injury occurs during coronary bypass
surgery once blood perfusion to the heart is restarted. Although the restoration of oxygen to ischemic myocardial cells is critical for tissue survival, reperfusion causes myocardial
oxidative stress, attributable in part to the increased production of
reactive oxygen species (ROS). Enhanced ROS production is associated
with mitochondrial damage. Adult female New Zealand white rabbits were
anesthetized and a left thoracotomy performed to expose the heart. The distal segment of the left
anterior descending coronary artery was occluded for 15 minutes and
then released so reperfusion of the tissue could occur. PRP (.21 mg/heart) or saline was injected into the ischemic area of the myocardium. Mechanical function of the left
ventricle was analyzed using a Millar catheter attached to a Micro-Med
Analysis System. H9c2 cells in culture were treated with 1 mL of nsPEF
activated PRP (1.05 mg/flask) for 24 hours before analysis for ROS
production or mitochondrial depolarization damage). The left ventricle contracted and relaxed faster and infarct size
was reduced in hearts treated with PRP compared with saline. ROS
production and mitochondrial depolarization were reduced in H9c2 cells
treated with PRP and stimulated with hydrogen peroxide. These results
provide evidence that nsPEFs can successfully be used to prepare PRP and
that the PRP is functional in heart protection possibly by reducing ROS generation and stabilizing the mitochondria of the ischemic/reperfused heart.