title: [Effect of sulodexide on aortic vasodilation capacity and associated morphological changes in rats with streptozotocin-induced diabetes].
abstract: Endothelial dysfunction (ED) is observed in patients with hypercholesterolemia, arterial hypertension, obesity and diabetes mellitus. Recent evidences suggest the involvement of glycosaminoglycans (GSG) in ED. We evaluated the effect of sulodexide (SLD), a natural GSG used in albuminuria and ischemic diabetes treatment, on arterial relaxation and vascular morphological changes in a diabetic type I model. Diabetes was induced, in Sprague-Dawley rats by streptozotocine (STZ) administration, 60 mg, i.v. Rats were divided into four groups; I: control, II: diabetics, III: control + SLD, IV: diabetics treated with SLD (15 mg/day). After three months, phenylephrine precontracted aortic rings were used to evaluate acetylcholine (ACh) and sodium nitroprusside (NPS) relaxation capacities. Light microscopy of aorta was done with several staining procedures. In vitro, SLD did not change smooth muscle tone in resting or phenylephrine precontracted aortic rings. In diabetic rats, ACh relaxation was 28.8-35.1% lower than in control rats. Diabetic rats treated with SLD showed aortic ACh relaxation similar to control rats. No significative statistical difference was found in endothelium-independent NPS relaxation, between the different groups. Light microscopy histological studies revealed important morphological alterations, particularly in intima and adventitia layers of aortic artery; those changes were dramatically reversed in SLD treated rats. Our experiments support the conclusion that SLD is a potential drug for improving endothelial dysfunction in diabetes.
authors.affiliation: Laboratorio de Estudios Cardiovasculares, Cátedra de Farmacología, Escuela de Medicina "José María Vargas", Facultad de Medicina, Universidad Central de Venezuela, Caracas, Venezuela. jovivas43@yahoo.es
authors.forename: José
authors.initials: J
authors.lastname: Vásquez
authors.forename: Yaira
authors.initials: Y
authors.lastname: Mathison
authors.forename: Eduardo
authors.initials: E
authors.lastname: Romero-Vecchione
authors.forename: Claudia
authors.initials: C
authors.lastname: Suárez
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D001018:Aortic Diseases / Q000209:etiology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D003925:Diabetic Angiopathies / Q000209:etiology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D004353:Drug Evaluation, Preclinical; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000648:ultrastructure; D006025:Glycosaminoglycans / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use*; D007004:Hypoglycemic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D009599:Nitroprusside / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017539:Tunica Intima / Q000187:drug effects / Q000648:ultrastructure; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D006025:Glycosaminoglycans; D007004:Hypoglycemic Agents; D009599:Nitroprusside; C007858:glucuronyl glucosamine glycan sulfate; D000109:Acetylcholine