LIPOPEROXIDATION AND VASCULAR REACTIVITY RESPONSE IN RAT MODELS OF STREPTOZOTOCININDUCED DIABETES MELLITUS

The murine model of streptozotocin-induced diabetes mellitus has been widely used for many authors. However, there are meaningful discrepancies about the functional alterations reported; especially regarding vascular response. Objective: The objective of the present study was to examine how the prolonged effects of diabetes mellitus induced by administering streptozotocin affects vascular reactivity, lipoperoxidation and endothelial function in aortic rings and if the administration of nicotinamide will partially protect those adverse outcomes. Performing parallel studies could contribute in part to clarify previous controversial results. Methods: Four groups (n= 8 rats per group) were used; control, control + Nicotinamide, streptozotocin or streptozotocin + Nicotinamide. Animals were euthanized after 20 weeks of streptozotocin and/or Nicotinamide administration. Glucose, lipoproteins plasma levels or lipid peroxidation in liver, heart and thoracic aorta were determined. Thoracic aorta was dissected and vascular reactivity to phenylephrine, isoproterenol, sodium nitroprusside or carbachol was determined. Results: Diabetic rats ingested more food and water, and lost more weight than control rats. The lipid peroxidation was higher in heart, liver and aorta in diabetic rats compared to control rats. In diabetic rats, total cholesterol, Low Density Lipoprotein and Triglyceride were higher and High Density Lipoprotein was lower than in control rats. The vasoconstrictor response to phenylephrine in streptozotocin groups was lower than streptozotocin + Nicotinamide and control groups. Diabetic animals showed a lower vasorelaxation response to carbachol and isoproterenol, but there was no significant difference in vascular response to sodium nitroprusside among groups. Conclusions: The prolonged effect of streptozotocin -induced diabetes increases chronically glycemia and alters vasodilator responses via different from the effect of oxidative stress. The partial protection with nicotinamide reduced vasomotor responses, suggesting that the artery is a major cause of the hypertensive status that characterizes the disease. Keywords: Diabetes; endothelial dysfunction, animal model