Low power laser irradiation of blood inhibits platelet function: Role of cyclic GMP

Alexander G. Brill*, Grigory E. Brill, Boris Shenkman, Ilya Tamarin, Rima Dardik, David Varon, Naphtali Savion

*Corresponding author for this work

Research output: Contribution to journalConference articlepeer-review


The aim of the present work was to investigate effect of low power laser irradiation (LPLI) on platelet function in vitro. He-Ne laser (Optronix, USA; λ-632.8 nm, output power-7 mW) was employed. Platelet adhesion and aggregation in whole blood (WB) under defined shear conditions were assayed by a Cone and Plate(let) Analyzer. Platelet activation was evaluated by flow cytometry. Level of platelet cGMP was estimated by immunoenzyme assay. Experiments performed showed that LPLI of WB resulted in decrease of platelet deposition on extracellular matrix (ECM) at high shear rate (1300 s-1). Similar results were obtained using surfaces precoated with either collagen type I or von Willebrand factor. LPLI inhibited fibrinogen binding as well as P-selectin expression on the platelet membrane, induced by thrombin analogue. It was found out that primary acceptor of laser energy responsible for the effect on platelets was located in platelets themselves and not in blood plasma or in other blood cells. LPLI of gel-filtered platelets resulted in increase of intracellular level of cGMP both in the absence and in presence of izobutylmethylxantine (phosphodiesterase inhibitor) suggesting stimulation of synthesis rather than destruction of cGMP under the influence of LPLI. It is suggested that guanylate cyclase and/or NO-synthase might serve as primary acceptors of He-Ne laser light in platelets.

Original languageEnglish
Pages (from-to)4-11
Number of pages8
JournalProceedings of SPIE - The International Society for Optical Engineering
StatePublished - 1999
Externally publishedYes
EventProceedings of the 1998 Effects of Low-Power Light on Biologigal Systems IV - Stockholm, SWE
Duration: 8 Sep 19989 Sep 1998


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