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Glucose infusion (3g/kg) increases nerve vascular conductance through an insulin‐mediated nitric oxide mechanism in rats
Author(s) -
Olver T Dylan,
Mattar Louis M,
Grise Ken N,
Twynstra Jasna,
Lacefield James C,
Noble Earl G,
Shoemaker J Kevin
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.853.19
Subject(s) - medicine , insulin , saline , nitric oxide , endocrinology , blood pressure , anesthesia , blood flow
We tested the hypothesis that acute hyperglycemia will reduce nerve vascular conductance (NVC) in rats. Sprague‐Dawley rats (N=25) were anaesthetised, blood pressure (MAP) was monitored with a pressure transducer and the left sciatic nerve was exposed from the dorsal side. Doppler ultrasound (40‐MHz: Vevo 2100 ‐ VisualSonics) was used to measure nerve blood flow velocity in an arterial segment along the nerve. Rats underwent one of four systemic intravenous glucose infusion protocols (1: 1g/kg body mass glucose; 2) 3g/kg glucose; 3) 3g/kg + 15mg/kg of L‐NAME and 4) 15mg/kg of L‐NAME alone + 3g/kg of glucose after 20min), as well as an isovolumetric saline infusion (saline did not affect NVC). An additional group was injected with streptozotocin (60mg/kg) with an insulin pellet implanted subcutaneously to produce a normoglycemic, non‐insulin responsive condition; these animals also underwent the 3g/kg glucose infusion. Relative to baseline 3g/kg increased (P<0.01) NVC (NBVF/MAP; ~ 125%). This dilation was blunted in the L‐NAME and non‐insulin responsive groups (both NS). Therefore, hyperglycemia‐induced increases in NVC appear to be mediated by an insulin‐stimulated NO mechanism. Funded by a CIHR