Tıp Fakültesi / Faculty of Medicine

Permanent URI for this collectionhttps://hdl.handle.net/11727/1403

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Author: search.filters.author.Aydingoz, Selda EmreHas files: Yes

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    Effects of Hypoxia Versus Ischaemia on Vascular Functions of Isolated Rat Thoracic Aorta: Revisiting the in Vitro Vascular Ischaemia/Reperfusion Model
    (2023) Orhan, Halit Guner; Teimoori, Ariyan; Demirtas, Elif; Zeynalova, Nargiz; Efe, Oguzhan Ekin; Aydingoz, Selda Emre; 37937174
    Introduction The in vitro rat vascular ischaemia and reperfusion model is used to evaluate the molecular and functional effects of potential agents against ischaemia and reperfusion injury of autologous graft veins. However, there is no consensus on whether hypoxia, rather than ischaemia, is sufficient to induce vascular dysfunction. Aim To compare the effects of hypoxia and ischaemia, with or without reperfusion, on the vascular functions of isolated thoracic aortic rings of rats. Material and methods Thoracic aortas of 12 male Sprague-Dawley rats (350-500 g, 18-24 months old) were isolated and divided into rings that were randomly allocated to control, ischaemia, hypoxia, ischaemia-reperfusion, and hypoxia-reperfusion groups. Aortic rings other than those of the control group were stored at 4 degrees C for 24 h in saline. For ischaemia, saline was gassed with nitrogen. After 24 h, aortic rings in the ischaemia-reperfusion and hypoxia-reperfusion groups were incubated with 200 mu M sodium hypochlorite for 30 min. Vascular and endothelial functions were tested in an organ bath set-up. Results Vascular response to potassium chloride (80 mM) decreased in all experimental groups compared to the control group (p = 0.007), but phenylephrine-induced contraction (10-5 M) increased only in the ischaemia-reperfusion group (p < 0.0001). Acetylcholine (10-11-10-5 M)-induced endothelium-dependent vasorelaxations were impaired in all groups - particularly in the ischaemia-reperfusion group (p = 0.0011). Sodium nitroprusside (10-12-10-7 M)-induced endothelium-independent vasorelaxations were similar across all groups (p = 0.1258). Conclusions Ischaemia followed by reperfusion should be implanted to achieve maximum endothelial and contractile dysfunction in vitro, and to replicate ischaemia and reperfusion injury of autologous graft veins.
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    Mechanism of acitretin-induced relaxations in isolated rat thoracic aorta preparations
    (2022) Efe, Oguzhan Ekin; Aydos, Tolga Resat; Aydingoz, Selda Emre; 0000-0002-3243-7843; 0000-0001-7823-7620; 34411501; W-7908-2019; ABA-4291-2020
    Acitretin is a member of vitamin A-derived retinoids, and its effect on vascular smooth muscle had not yet been studied. The aim of this study is to investigate the effect of acitretin, a retinoid, on vascular smooth muscle contractility. Thoracic aorta preparations obtained from 34 male Sprague-Dawley rats (355 +/- 15 g) were studied in isolated organ baths containing Krebs-Henseleit solution. The relaxation responses were obtained with acitretin (10-12-10-4 M) in endotheliumpreserved and endothelium-denuded aorta preparations precontracted with submaximal concentration of phenylephrine (10-6 M). The role of retinoic acid receptors (RARs), nitric oxide, adenylyl, and guanylyl cyclase enzymes, and potassium channels in these relaxation responses were investigated. Acitretin produced concentration-dependent relaxations, which were independent of its solvent dimethylsulfoxide (DMSO), in endothelium-denuded phenylephrine-precontracted thoracic aorta preparations. While incubation with the RAR antagonist (AGN193109, 10-5 M) had no effect on these relaxations; nitric oxide synthase inhibitor (L-NG-Nitro arginine methyl ester (L-NAME), 10-4 M), adenylyl cyclase inhibitor (SQ2253, 10-5 M), guanylyl cyclase inhibitor (oxadiazolo [4,3-a] quinoxalin-1-one (ODQ), 10-6 M), and potassium channel blocker (tetraethylammonium (TEA), 10-2 M) significantly eliminated the relaxation responses induced by acitretin. Acitretin induces relaxation in rat isolated thoracic aorta preparations without endothelium, which may be mediated by nitric oxide, cyclic adenosine monophosphate, and cyclic guanosine monophosphate-dependent kinases and potassium channels.