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In vitro effects of acute exposure to hyperglycemic conditions on endothelium‐dependent vasodilation in mourning doves ( Zenaida macroura )
Author(s) -
Jarrett Catherine L,
Sweazea Karen L
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.886.7
Subject(s) - vasodilation , medicine , vasoconstriction , endocrinology , phenylephrine , endothelium , acetylcholine , mannitol , anatomy , chemistry , blood pressure , biochemistry
Normal avian plasma glucose levels are 1.5–2 times greater than mammals of similar size. In mammals, hyperglycemia leads to endothelial dysfunction and impaired vasodilation. The hypothesis was that endothelium‐dependent vasodilation of isolated avian arteries would not be impaired following acute exposure to high glucose. Isolated small resistance saphenous arteries (80–150μm, inner diameter) were cannulated and pressurized in a vessel chamber then incubated with a ringer 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). Pre‐exposure of high glucose arteries to the superoxide dismutase mimetic tiron (10mM) improved vasodilation ( p <0.05). Therefore, dove arteries do not appear to have endogenous mechanisms to prevent impaired vasodilation resulting from high glucose