Oxidative stress impairs vasodilation of ex vivo arteries from mourning doves (Z. macroura) (880.3)

Abstract

In mammals, high plasma glucose concentrations (PGlu) lead to oxidative stress‐induced endothelial dysfunction and impaired vasodilation. However, avian PGlu are normally 1.5‐2 times greater than mammals of similar size. 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 (80‐150μm, inner diameter) were cannulated and pressurized in a vessel chamber then incubated with a physiological solution containing 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) and exposed to increasing doses of acetylcholine (ACh; 10‐9 to 10‐5 M, 5 mins per step). Percent reversal of PE‐induced tone 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 a combination of 20mM glucose and 10mM mannitol was not different from controls (p=0.898). Superoxide concentrations were significantly increased in arteries exposed to high glucose (168 ± 42%, p = 0.0072) and pre‐exposure of arteries to the superoxide dismutase mimetic tiron (10mM) improved vasodilation (p<0.05). Therefore, dove arteries are subject to oxidative stress‐mediated pathologies in conditions mimicking hyperglycemia.