Microparticle levels after arterial injury and NO therapy in diabetes

Abstract

BackgroundLittle is known about how arterial injury, nitric oxide (NO), or the diabetic milieu impact microparticle (MP) levels in the vasculature. We hypothesized that MP levels would increase following local arterial injury, and that NO would modify MP levels differently based on the metabolic environment. Materials and methodsType 1 diabetes was induced in male Lean Zucker (LZ) rats with streptozotocin, and type 2 diabetes was induced in male Zucker diabetic fatty rats through diet. Lean Zucker rats served as nondiabetic controls. The rat carotid balloon injury was performed ± NO (n > 4/group). Blood was obtained at intervals from baseline to 14 d after injury and analyzed for platelet MP (PMP), leukocyte MP (LMP), and endothelial MP (EMP) using fluorescence-activated cell sorting (FACS) analysis. ResultsAt baseline, type 1 diabetic rats had the highest EMP levels (P < 0.05). After arterial injury, type 1 and type 2 diabetic rats had a transient increase in EMP levels (P < 0.05) before decreasing below baseline levels. Both LMP and PMP levels generally declined after injury in all three animal models but were the lowest in both type 1 and type 2 diabetic rats. NO therapy had little impact on MP levels in nondiabetic and type 1 diabetic rats after injury. Conversely, NO caused a dramatic increase in EMP, LMP, and PMP levels in type 2 diabetic animals at early time points after injury (P < 0.05). ConclusionsThese data demonstrate that the diabetic milieu impacts MP levels at baseline, after arterial injury and with NO treatment.