Blue Laser Light Increases Perfusion of a Skin Flap Via Release of Nitric Oxide from Hemoglobin

Rainer Mittermayr,Carina Weber,Anatoly Osipov,Christina Piskernik,Heinz Redl,Yuri A Vladimirov,Peter Dungel,Susanne Haindl,Andrey V Kozlov

doi:10.2119/2006-00035.mittermayr

Abstract

It has recently been shown that nitrosyl complexes of hemoglobin (NO-Hb) are sensitive to low-level blue laser irradiation, suggesting that laser irradiation can facilitate the release of biologically active nitric oxide (NO), which can affect tissue perfusion. The aim of this study was to evaluate the therapeutic value of blue laser irradiation for local tissue perfusion after surgical intervention. Blood was withdrawn from a rat, exposed to NO and infused back to the same rat or used for in vitro experiments. In vitro, an increase of NO-Hb levels (electron paramagnetic resonance spectroscopy) up to 15 microM in rat blood did not result in the release of detectable amounts of NO (NO selective electrode). Blue laser irradiation of NO-Hb in blood caused decomposition of NO-Hb complexes and release of free NO. Systemic infusion of NO-Hb in rats affected neither systemic circulation (mean arterial pressure) nor local tissue perfusion (Doppler blood flow imaging system). In contrast, a clear enhancement of local tissue perfusion was observed in epigastric flap when elevated NO-Hb levels in blood were combined with local He-Cd laser irradiation focused on the left epigastric artery. The enhancement of regional tissue perfusion was not accompanied by any detectable changes in systemic circulation. This study demonstrates that blue laser irradiation improves local tissue perfusion in a controlled manner stimulating NO release from NO-Hb complexes.

Highlights

Decreased peripheral blood flow related to impaired microcirculatory vasodilatation has been shown to occur in certain disease states including peripheral vascular disease, diabetes mellitus, hypercholesterolemia, hypertension, chronic renal failure, abdominal aortic aneurysmal disease, and venous insufficiency, as well as in menopause, advanced age, and obesity [1]
Gow and coauthors [12,13], have shown that oxygen drives the conversion of nitrosylhemoglobin to S-nitrosohemoglobin (SNO-Hb), which was suggested to act as an endogenous Nitric oxide (NO) donor and physiological regulator of blood pressure, releasing NO [14]
To prove that nitrosyl complexes of hemoglobin (NO-Hb) is decreasing due to laser exposure, we looked at the samples incubated a total of 2 min with different exposure times

Summary

Introduction

Decreased peripheral blood flow related to impaired microcirculatory vasodilatation has been shown to occur in certain disease states including peripheral vascular disease, diabetes mellitus, hypercholesterolemia, hypertension, chronic renal failure, abdominal aortic aneurysmal disease, and venous insufficiency, as well as in menopause, advanced age, and obesity [1]. The main source of NO for vasodilatation is the endothelial NO synthase (eNOS) The expression of this enzyme is regulated by a range of transcriptional and posttranscriptional mechanisms generating NO in response to a number of stimuli [9]. NO reacts quickly with Hb. In blood, NO reacts quickly with Hb This interaction follows two pathways, namely NO-mediated oxidation of oxyHb to methemoglobin yielding NO3and, secondly, the binding of NO to Hb yielding nitrosyl complexes of hemoglobin (NO-Hb). Both reactions have very high rate constants, 3.7 × 107 M-1 s-1 and 2.6 × 107 M-1 s-1, respectively [12], suggesting that under physiological conditions, there is no free NO in blood. Despite these conflicting data on the role of SNO-Hb, the NO-Hb complexes are not considered to be a source of NO due to very high affinity of NO to heme iron

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