| Autor: |
Ors Yildirim N; Department of Anesthesiology and Reanimation, Sincan Training and Research Hospital, Ankara 06949, Turkey., Yildirim AK; Department of Cardiovascular Surgery, Faculty of Medicine, Gazi University, Ankara 06560, Turkey., Demeli Ertus M; Department of Physiology, Zonguldak Bulent Ecevit University, Zonguldak 67600, Turkey., Dastan AO; Department of Physiology, Hacettepe University Faculty of Medicine, Ankara 06100, Turkey., Pehlivanoglu B; Department of Physiology, Hacettepe University Faculty of Medicine, Ankara 06100, Turkey., Chi YW; Vascular Center, University of California, Sacramento, CA 95817, USA., Gianesini S; Department of Surgery, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA., Doganci S; Vein Vascular Clinics, Ankara 06510, Turkey., Yildirim V; Department of Anesthesiology and Reanimation, Gulhane Training and Research Hospital, University of Health Sciences, Ankara 06010, Turkey. |
| Abstrakt: |
Background/Objectives : Sulodexide (SDX) is a drug known for restoring the glycocalyx, thereby offering endothelial protection and regulating permeability. Additionally, it has antithrombotic and anti-inflammatory properties and has shown arterial vasodilatory effects. Endothelial cells play a crucial role in maintaining homeostasis, with their dysfunction being a key contributor to loss in vasodilatory response, especially in arterial pathologies. The aim of this study was to investigate the effects of SDX on stimulated vascular tonus in human arterial samples and to assess the function of the endothelial layer as a source of nitric oxide (NO). Methods : A total of 16 internal mammary artery remnants from coronary artery bypass graft surgeries were dissected into endothelium-intact and endothelium-denuded groups (n = 8 each). The arterial rings were equilibrated under tension, with their basal tonus recorded before and after phenylephrine stimulation. SDX's impact on arterial contraction was assessed through cumulative dose-response curves. NO synthase inhibitor (Nω-nitro-L-arginine methyl ester) was used to assess SDX's vasodilatory effect over the NO pathway. Results : SDX application resulted in concentration-dependent vasorelaxation in both endothelium-intact and endothelium-denuded groups at certain doses. However, the inhibitory effect of SDX was more pronounced in endothelium-intact rings at higher doses compared to endothelium-denuded rings ( p < 0.05). Similar inhibition of contraction curves was achieved for both endothelium-intact and endothelium-denuded rings after L-NAME pre-incubation, suggesting a necessity for NO-related endothelial pathways. Conclusions : SDX exerts a concentration-dependent inhibition on arterial contraction, emphasizing the critical role of an intact endothelium and NO-mediated pathways in this process. This underscores SDX's potential in treating endothelial dysfunction-related pathologies. |
