NO released from EXISTING NO STORES when stimulated by LLLT

As we know, one of the first responses to LED and Laser light absorption is release of or production of Nitric Oxide (NO) and that this reactive molecule modulates a cascade of secondary biological responses ultimately resulting in cytoprotection and/or gross physiological change, (particularly in stressed / hypoxic tissues).

In the current issue of J Molec Cell Cardiol, Zhang and colleagues utilize cultured cardiomyocytes subjected to hypoxia and reoxygenation to demonstrate that 5 min of NIR treatment upon reoxygenation  protects the cells from injury and eventual death and that this cytoprotection is dependent on the release of nitric oxide.

but how? read on

Shining a light on tissue NO stores: Near infrared release of NO from nitrite and nitrosylated hemes

In recent years it has been shown that light in the red to near infrared (NIR) region, generated by a low energy laser or light emitting diodes, can modulate a number of biological responses including wound healing [1,2], angiogenesis [1,3], and cytoprotection after ischemia/reperfusion (I/R) [4]. Although the applications of NIR have expanded rapidly, the exact molecular mechanisms underlying these cytoprotective effects remain unknown. In the current issue of J Molec Cell Cardiol, Zhang and colleagues utilize cultured cardiomyocytes subjected to hypoxia and reoxygenation to demonstrate that 5 min of NIR treatment upon reoxygenation (analogous to post conditioning) protects the cells from injury and eventual death [5]. Mechanistically, they demonstrate that this cytoprotection is dependent on the release of nitric oxide (NO), as the NO scavengers carboxy-PTIO and oxyhemoglobin inhibit NIR-mediated cytoprotection. Interestingly, although the authors show that DAF fluorescence increases in the cell after NIR treatment, indicative of increased NO, the cytoprotective effect of NIR is only partially inhibited by the nitric oxide synthase (NOS) inhibitor L-NMMA, suggesting that at least a fraction of the NO release is independent of enzymatic NO formation by NOS. Hence, the authors reason that NIR stimulates NO release from existing NO stores within the tissue [5].

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=18992252[uid]