TY - GEN
T1 - Light therapy for the cardiovascular system
AU - Tuby, Hana
AU - Maltz, Lydia
AU - Oron, Uri
PY - 2008
Y1 - 2008
N2 - Coronary artery disease, which may lead to myocardial infarction (MI), is the primary cause of mortality world-wide. In a series of studies in which the rat and canine models were used, the effect of LLLT on infarct size after chronic myocardial infarction in rats was investigated. LLLT caused a profound (50-70%) reduction in infarct size and ventricular dilatation in the rat heart after chronic MI. This phenomenon was achieved by the cardioprotective effect of LLLT on mitochondria, elevation of cytoprotective heat shock proteins and enhanced angiogenesis in the myocardium following laser irradiation. The effect of LLLT on the expression of vascular endothelial growth factor (VEGF) and inducible nitric oxide synthase (iNOS) in the infarcted heart was also investigated. It was found that VGEF and iNOS expression in the infarcted rat heart is markedly upregulated by LLLT and is associated with enhanced angiogenesis and cardioprotection. The possible beneficial effects on implantation of autologeous mesenchymal stem cells (MSCs) that had been laser irradiated prior to their implantation into the infarcted rat heart was also investigated. These findings provided the first evidence that LLLT can significantly increase survival and/or proliferation of MSCs post implanation into the ischemic/ infarcted heart, followed by a marked reduction of scarring, and enhanced angiogenesis. The results of the animal studies may also have clinical relevance. It can be postulated that the use of laser following MI is most probably safe and our observations indicate that delivery of laser energy to the heart may have an important beneficial effect on patients after acute MI or ischemic heart conditions.
AB - Coronary artery disease, which may lead to myocardial infarction (MI), is the primary cause of mortality world-wide. In a series of studies in which the rat and canine models were used, the effect of LLLT on infarct size after chronic myocardial infarction in rats was investigated. LLLT caused a profound (50-70%) reduction in infarct size and ventricular dilatation in the rat heart after chronic MI. This phenomenon was achieved by the cardioprotective effect of LLLT on mitochondria, elevation of cytoprotective heat shock proteins and enhanced angiogenesis in the myocardium following laser irradiation. The effect of LLLT on the expression of vascular endothelial growth factor (VEGF) and inducible nitric oxide synthase (iNOS) in the infarcted heart was also investigated. It was found that VGEF and iNOS expression in the infarcted rat heart is markedly upregulated by LLLT and is associated with enhanced angiogenesis and cardioprotection. The possible beneficial effects on implantation of autologeous mesenchymal stem cells (MSCs) that had been laser irradiated prior to their implantation into the infarcted rat heart was also investigated. These findings provided the first evidence that LLLT can significantly increase survival and/or proliferation of MSCs post implanation into the ischemic/ infarcted heart, followed by a marked reduction of scarring, and enhanced angiogenesis. The results of the animal studies may also have clinical relevance. It can be postulated that the use of laser following MI is most probably safe and our observations indicate that delivery of laser energy to the heart may have an important beneficial effect on patients after acute MI or ischemic heart conditions.
KW - Angiogenesis
KW - Cardioprotection
KW - Heart muscle
KW - Low level laser irradiation
UR - http://www.scopus.com/inward/record.url?scp=84884990519&partnerID=8YFLogxK
U2 - 10.1007/978-0-387-71809-5_14
DO - 10.1007/978-0-387-71809-5_14
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AN - SCOPUS:84884990519
SN - 9780387718088
T3 - Lecture Notes in Electrical Engineering
SP - 151
EP - 156
BT - Proceedings of Light-Activated Tissue Regeneration and Therapy Conference
T2 - 2nd Conference on "Light-Activated Tissue Regeneration and Therapy" an Engineering Conference International, ECI 2007
Y2 - 24 June 2007 through 29 June 2007
ER -