Light-Induced Vasodilation of Coronary Arteries and Its Possible Clinical Implication

Plass, Christian; Loew, H; Podesser, Bruno K.; Prusa, Alexander M.

doi:10.1016/j.athoracsur.2011.12.062

Cited by 37 publications

(24 citation statements)

References 22 publications

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“…These results suggest the presence of a preformed and finite store within the vessel which could produce vasodilation. Porcine coronary artery rings exposed to 10 J/cm 2 of 670 nm light energy [12] produced results similarly to Batenberg et al [11]. However, in our study, we found murine vessels incubated at a physiological pressure will dilate in response to light in a time dependent manner, and upon discontinuation of light, vessel diameter decreased or plateaued.…”

Section: Discussionsupporting

confidence: 80%

“…In addition, we have shown that R/NIR irradiation can stimulate collateral vessel growth after occlusion [10]. While R/NIR light has consistently been shown to stimulate the dilation of blood vessels in various vascular beds and preparations, and largely through NO-dependent processes, the fundamental mechanism of action of light remains unknown [11, 12]. The consequences of these observations are relevant to vascular pathologies where NO bioavailability is impaired and particularly in diabetic vasculopathy where current treatments often involve surgery and amputation.…”

Section: Introductionmentioning

confidence: 99%

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Red/near infrared light stimulates release of an endothelium dependent vasodilator and rescues vascular dysfunction in a diabetes model

Keszler

Lindemer

Weihrauch

et al. 2017

Free Radical Biology and Medicine

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Peripheral artery disease (PAD) is a morbid condition whereby ischemic peripheral muscle causes pain and tissue breakdown. Interestingly, PAD risk factors, e.g. diabetes mellitus, cause endothelial dysfunction secondary to decreased nitric oxide (NO) levels, which could explain treatment failures. Previously, we demonstrated 670nm light (R/NIR) increased NO from nitrosyl-heme stores, therefore we hypothesized R/NIR can stimulate vasodilation in healthy and diabetic blood vessels. Vasodilation was tested by ex vivo pressure myography in wild type C57Bl/6, endothelial nitric oxide synthase (eNOS) knockout, and db/db mice (10 mW/cm2 for 5min with 10 min dark period). NOS inhibition with N-Nitroarginine methyl ester (L-NAME) or the NO scavenger Carboxy-PTIO (c-PTIO) tested the specificity of NO production. 4,5-Diaminofluorescein diacetate (DAF-2) measured NO in human dermal microvascular endothelial cells (HMVEC-d). R/NIR significantly increased vasodilation in wild type and NOS inhibited groups, however R/NIR dilation was totally abolished with c-PTIO and blood vessel denudation. Interestingly, the bath solution from intact R/NIR stimulated vessels could dilate light naïve vessels in a NO dependent manner. Characterization of the bath identified a NO generating substance suggestive of S-nitrosothiols or non heme iron nitrosyl complexes. Consistent with the finding of an endothelial source of NO, intracellular NO increased with R/NIR in HMVEC-d treated with and without L-NAME (1mM), yet c-PTIO (100μm) reduced NO production. R/NIR significantly dilated db/db blood vessels. In conclusion, R/NIR stimulates vasodilation by release of NO bound substances from the endothelium. In a diabetes model of endothelial dysfunction, R/NIR restores vasodilation, which lends the potential for new treatments for diabetic vascular disease.

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Section: Discussionsupporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Red/near infrared light stimulates release of an endothelium dependent vasodilator and rescues vascular dysfunction in a diabetes model

Keszler

Lindemer

Weihrauch

et al. 2017

Free Radical Biology and Medicine

View full text Add to dashboard Cite

show abstract

“…Plass et al show in two studies that LLLT with red light leads to significant relaxation of aortic rings and that this relaxation is mediated by NO as it is inhibited by 2‐(4‐carboxyphenyl)‐4,4,5,5‐tetramethylimidazoline‐1‐oxyl‐3‐oxide, a specific nitric oxide scavenger, and 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one, a specific guanocyclase inhibitor, but not by L ‐nitro‐arginine methyl ester or deendothelialization . It has been shown that NO stimulates angiogenesis via stimulation of VEGF expression.…”

Section: Discussionmentioning

confidence: 99%

Low level light therapy by LED of different wavelength induces angiogenesis and improves ischemic wound healing

et al. 2014

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“…Furthermore, LLI can also result in the release of bound nitric oxide from CCO (Karu et al, 2005). These effects in combination lead to a range of effects, including increased ATP content (Karu et al, 1995), altered mitochondrial dynamics (Pastore et al, 1994), apparent vasodilation (Plass et al, 2012), and inflammation mitigation (Muili et al, 2012). LLI has shown beneficial effects in models of stroke (Huisa et al, 2013), traumatic brain injury (Xuan et al, 2014), and Parkinson’s disease (Ying et al, 2008) by ameliorating neuronal damage and improving behavioral outcomes.…”

Section: Introductionmentioning

confidence: 99%

Low-level laser therapy for beta amyloid toxicity in rat hippocampus

Wang

Dong

et al. 2017

Neurobiology of Aging

134

177

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Beta amyloid (Aβ) is well accepted to play a central role in the pathogenesis of Alzheimer’s disease (AD). The present work evaluated the therapeutic effects of low-level laser irradiation (LLI) on Aβ-induced neurotoxicity in rat hippocampus. Aβ 1–42 was injected bilaterally to the hippocampus CA1 region of adult male rats, and 2-minute daily LLI treatment was applied transcranially after Aβ injection for 5 consecutive days. LLI treatment suppressed Aβ-induced hippocampal neurodegeneration and long-term spatial and recognition memory impairments. Molecular studies revealed that LLI treatment: (1) restored mitochondrial dynamics, by altering fission and fusion protein levels thereby suppressing Aβ-induced extensive fragmentation; (2) suppressed Aβ-induced collapse of mitochondrial membrane potential; (3) reduced oxidized mitochondrial DNA and excessive mitophagy; (4) facilitated mitochondrial homeostasis via modulation of the Bcl-2-associated X protein/B-cell lymphoma 2 ratio and of mitochondrial anti-oxidant expression; (5) promoted cytochrome c oxidase activity and adenosine triphosphate synthesis; (6) suppressed Aβ-induced glucose-6-phosphate dehydrogenase and nicotinamide adenine dinucleotide phosphate oxidase activity; (7) enhanced the total antioxidant capacity of hippocampal CA1 neurons, whereas reduced the oxidative damage; and (8) suppressed Aβ-induced reactive gliosis, inflammation, and tau hyperphosphorylation. Although development of AD treatments has focused on reducing cerebral Aβ levels, by the time the clinical diagnosis of AD or mild cognitive impairment is made, the brain is likely to have already been exposed to years of elevated Aβ levels with dire consequences for multiple cellular pathways. By alleviating a broad spectrum of Aβ-induced pathology that includes mitochondrial dysfunction, oxidative stress, neuroinflammation, neuronal apoptosis, and tau pathology, LLI could represent a new promising therapeutic strategy for AD.

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Light-Induced Vasodilation of Coronary Arteries and Its Possible Clinical Implication

Cited by 37 publications

References 22 publications

Red/near infrared light stimulates release of an endothelium dependent vasodilator and rescues vascular dysfunction in a diabetes model

Red/near infrared light stimulates release of an endothelium dependent vasodilator and rescues vascular dysfunction in a diabetes model

Low level light therapy by LED of different wavelength induces angiogenesis and improves ischemic wound healing

Low-level laser therapy for beta amyloid toxicity in rat hippocampus

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