کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1971833 | 1538986 | 2016 | 5 صفحه PDF | دانلود رایگان |
Normal avian plasma glucose levels are 1.5–2 times greater than mammals of similar size. In mammals, hyperglycemia induces oxidative stress and impaired endothelium-dependent vasodilation. Prior work has shown that mourning doves have high levels of antioxidants and isolated vessels have low endogenous oxidative stress. Therefore, the hypothesis was that endothelium-dependent vasodilation of isolated avian arteries would not be impaired following acute exposure to high glucose. Isolated small resistance cranial tibial arteries (c. tibial) were cannulated and pressurized in a vessel chamber then incubated with either normal or high glucose (20 mM vs. 30 mM) for 1 h at 41 °C. Vessels were then pre-constricted to 50% of resting inner diameter with phenylephrine (PE) followed by increasing doses of acetylcholine (ACh; 10− 9 to 10− 5 M, 5 min per step). Percent vasodilation was measured by tracking the inner diameter with edge-detection software. Contrary to our hypothesis, ACh-induced vasodilation was impaired with acute exposure to high glucose (p = 0.013). The impairment was not related to increased osmolarity since vasodilation of arteries exposed to an equimolar combination of 20 mM d-glucose and 10 mM l-glucose was not different from controls (p = 0.273). Rather, the impaired vasodilation was attributed to oxidative stress since superoxide levels were elevated 168 ± 42% (p = 0.02) and pre-exposure of arteries to the superoxide dismutase mimetic tiron (10 mM) improved vasodilation (p < 0.05). Therefore, isolated arteries from doves do not have endogenous mechanisms to prevent impaired vasodilation resulting from high glucose-mediated increases in oxidative stress.
Journal: Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology - Volume 201, November 2016, Pages 141–145