Introduction: Venous wall weakness is supposed to be the most probable reason of primary varicosis. There are conflicting findings in literature about its structural changes. NO is potent vasodilatator due to the smooth muscle relaxation. It is synthesized by nitric oxide synthase (NOS). There are 3 known isoforms of NOS: nNOS (neuronal NOS), iNOS (inducible NOS), eNOS (endothelial NOS).
Material and methods: 10 varicose vein and 10 control vein samples were processed by standard light microscopy method. Sections were then processed by standard immuno-histochemic technique using rabbit polyclonal antibodies against all 3 NOS isoforms: iNOS, eNOS (SantaCruz, USA), nNOS (BioScience, USA). Antibodies expression was evaluated semiquantitatively and then proved morphometricaly by 2D image analysis (ImageJ 1.34n, National Institute of Health, USA). Total area of NOS isoforms expressions was determined by color analysis and color digital substraction.
Results: Histomorphological and semi quantitative evaluation of NOS isoforms showed discontinuous and significantly lower expression of all 3 NOS isoforms in tunica media of varicose veins compared with control group, where the expression of all 3 NOS isoforms was continuous. For the statistical analysis unpaired t-test was used.
Discussion and conclusion: Our results suppose lower NO levels in varicose vein wall, deducing that varicose vasodilatation is due to other mechanism, although the stage of chronic venous disease of varicose vein samples was undetermined. Our results are in contradiction with previously published results of Howlader et al., who observed raised total NO levels in patients with severe stages of chronic venous disease(Tab. 2, Fig. 13, Ref. 18).