Abstract 1904: Myocardial Postconditioning Against Ischemia and Reperfusion Injury by Near Infrared Electromagnetic Radiation
Near-infrared electromagnetic radiation (NIR) has been reported to stimulate biochemical processes within cells and tissue, but whether NIR is capable of acutely protecting myocardium against ischemia+reperfusion injury in vivo is unknown. We tested the hypothesis that NIR (670 nm, 30 nm bandwith, 50 mW/cm2) exposure immediately before and during early reperfusion protects rabbit myocardium against infarction that is dependent upon reactive oxygen species (ROS), nitric oxide synthase (NOS), mitochondrial KATP (mito KATP) channels and inhibition of mitochondrial permeability transition pore (mPTP) opening. Rabbits subjected to a 30 min left anterior descending coronary artery occlusion and reperfusion received no irradiation (control) or continuous NIR (beginning 3 min before and ending 7 min after reperfusion) in the presence or absence of ROS scavengers [N-acetylcysteine (NAC; 150 mg/kg), or tempol (30 mg/kg)], nonselective NOS inhibitor L-nitro-arginine methyl ester (L-NAME; 10 mg/kg), selective mitoKATP channel antagonist 5-hydroxydecanoate (5-HD; 10 mg/kg) or mPTP opener atractyloside (5 mg/kg). Dihydroethidium and diaminofluroscein immunofluorescence were used to detect ROS and NO production, respectively, in additional rabbits with or without NIR exposure. NIR reduced infarct size (24±4% of the area at risk; triphenyltetrazolium chloride staining) compared with control (46±3%). NAC, tempol, L-NAME, 5-HD, and atractyloside alone did not affect infarct size, but these drugs abolished the cardioprotective effect of NIR. NIR increased ROS production independent of ischemia and reperfusion, and this effect was blocked by NAC. NIR also enhanced NO generation during early reperfusion. In addition, NIR increased ATP synthesis in isolated rabbit mitochondria. Thus, NIR postconditions myocardium against infarction concomitant with ROS and NO production. MitoKATP channels and mPTP mediate cardioprotection by NIR.