Jarrett Catherine L, Ahmed Zoha, Faust James J, Sweazea Karen L
School of Nutrition and Health Promotion, Arizona State University, Phoenix, AZ, USA.
School of Life Sciences, Arizona State University, Tempe, AZ, USA.
Comp Biochem Physiol A Mol Integr Physiol. 2016 Nov;201:141-145. doi: 10.1016/j.cbpa.2016.07.010. Epub 2016 Jul 19.
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 (20mM vs. 30mM) for 1h 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, 5min 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 20mM d-glucose and 10mM 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 (10mM) 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.
正常鸟类血浆葡萄糖水平比体型相似的哺乳动物高1.5至2倍。在哺乳动物中，高血糖会诱导氧化应激并损害内皮依赖性血管舒张。先前的研究表明，哀鸽具有高水平的抗氧化剂，且分离出的血管内源性氧化应激水平较低。因此，提出的假设是，急性暴露于高血糖后，分离出的鸟类动脉的内皮依赖性血管舒张不会受到损害。将分离出的小型阻力性颅侧胫动脉（胫动脉）插管并在血管腔内加压，然后在41°C下用正常葡萄糖或高葡萄糖（20mM对30mM）孵育1小时。然后用去氧肾上腺素（PE）将血管预收缩至静息内径的50%，随后增加乙酰胆碱（ACh；10⁻⁹至10⁻⁵M，每步5分钟）的剂量。通过边缘检测软件跟踪内径来测量血管舒张百分比。与我们的假设相反，急性暴露于高血糖会损害ACh诱导的血管舒张（p = 0.013）。这种损害与渗透压升高无关，因为暴露于20mM d-葡萄糖和10mM l-葡萄糖等摩尔组合的动脉的血管舒张与对照组无差异（p = 0.273）。相反，血管舒张受损归因于氧化应激，因为超氧化物水平升高了168±42%（p = 0.02），并且动脉预先暴露于超氧化物歧化酶模拟物替诺（10mM）可改善血管舒张（p < 0.05）。因此，来自鸽子的分离动脉没有内源性机制来预防高血糖介导的氧化应激增加导致的血管舒张受损。
