Enhancement of nitric oxide release from nitrosyl hemoglobin and nitrosyl myoglobin by red/near infrared radiation: Potential role in cardioprotection

Abstract

Nitric oxide is an important messenger in numerous biological processes, such as angiogenesis, hypoxic vasodilation, and cardioprotection. Although nitric oxide synthases (NOS) produce the bulk of NO, there is increasing interest in NOS independent generation of NO in vivo, particularly during hypoxia or anoxia, where low oxygen tensions limit NOS activity. Interventions that can increase NO bioavailability have significant therapeutic potential. The use of far red and near infrared light (R/NIR) can reduce infarct size, protect neurons from methanol toxicity, and stimulate angiogenesis. How R/NIR modulates these processes in vivo and in vitro is unknown, but it has been suggested that increases in NO levels are involved. In this study we examined if R/NIR light could facilitate the release of NO from nitrosyl heme proteins. In addition, we examined if R/NIR light could enhance the protective effects of nitrite on ischemia and reperfusion injury in the rabbit heart. We show both in purified systems and in myocardium that R/NIR light can decay nitrosyl hemes and release NO, and that this released NO may enhance the cardioprotective effects of nitrite. Thus, the photodissociation to NO and its synergistic effect with sodium nitrite may represent a noninvasive and site specific means for increasing NO bioavailability.

Cardioprotection from Ischemia-Reperfusion Injury by Near-Infrared Light in Rats

“…Decreases in infarct size related to NIR treatment ranged from 33% to 77% compared with controls. These reductions in infarct size are similar to the cardioprotection afforded by a variety of pharmaceutical and nonpharmaceutical methods of preand post-ischemia conditioning, [31][32][33][34] including application of 803 nm laser light in a canine in vivo model. 19 The infarct size reduction seen in the in vivo model but not in the isolated heart model points to the possible involvement of some blood-borne element in NIR-mediated cardioprotection, as the isolated heart is perfused with bicarbonate buffer, or to a fundamental difference between the isolated global ischemia model and the in vivo regional ischemia animal model.…”

“…34 Under hypoxic conditions, hemoglobin or myoglobin can reduce nitrite to NO, and then capture this NO in a heme-nitrosyl complex. These complexes are kinetically stable, with slow off-rates.…”

Transcranial Low-Level Laser (Light) Therapy for Brain Injury

“…In turn, both ATP levels and blood flow increase (NO is a vasodilator). 24 With an increase in blood flow, improved oxygenation is found in damaged areas of the brain. Figure 1 depicts the molecular mechanisms and signaling pathways that are thought to occur post-LLLT.…”

Biophysical Approaches for Oral Wound Healing: Emphasis on Photobiomodulation

“…46 Broadly, the released NO has been shown to promote potent wound healing responses, such as in keratinocyte and tenocyte proliferation, endothelial migration and lumenization, macrophage function, angiogenesis in ischemic limb injuries, reduction of reperfusion injury, and vasodilation, and promote stem cell differentiation, among others. [47][48][49][50][51][52] Kinases, enzymes, hormones, and growth factor: Among its many biological targets, PBM (632 nm)-generated ROS has been shown to activate Src that has potent effects on cell proliferation, attachment, migration, and survival. 53 Src is a nonreceptor tyrosine kinase that can interact with a large number of biological pathways, including EGF, MAPK, FAK, and STAT3, among others.…”