Myocardial ischemic reperfusion (MIR) injury results from coronary revascularization and cardiac intervention procedures. It is a negative pathophysiological event that may result in cardiac cell apoptosis. The resulting loss of cardiomyocyte cells and the formation of scar tissue, impair heart function and this is a major prognostic determinant of long-term cardiac outcomes. Photobiomodulation (PBM) is potential cardiac surgery intervention that could prevent myocardial ischemic reperfusion related myocardial injury. A growing body of evidence supporting the use of photobiomodulation in myocardial infarct models (tissues, animal models and a limited number of clinical trials) has implicated multiple molecular pathways of PBM action. PBM has been shown to decrease infarct size, both when delivered transthoracically and to remote areas of the body. PBM has also been shown to decrease the complications of hearts surgery including arrhythmias, to reduced restenosis, to accelerate wound healing, both superficial and deep, and to improve subjective well-being.
One important factor in negative impact of injury is the spread of proteotoxic stress across compartments within the cell and across tissues. PBM is known to modify redox stress, to alter membrane ion channel stability, to affect cytoskeleton rescue and catastrophe and to alter the fluidity and stability of membranes and lipid rafts. A simple window into this is erythrocytes stability. The use of this measurement will be discussed, including its relevance to cardiac injury and its modification by PBM and the broader implications of the importance of PBM to cardioprotection and neuroprotection.
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